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Saturday, November 6, 2010

Association between Bell's palsy in pregnancy and pre‐eclampsia

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Association between Bell's palsy in pregnancy and pre‐eclampsia

  1. D. Shmorgun,
  2. W.‐S. Chan and
  3. J.G. Ray

+ Author Affiliations

  1. From the Department of Medicine, Sunnybrook and Women's College Health Science Centre, Toronto, Ontario, Canada
  • Received March 6, 2002.
  • Revision received March 12, 2002.


Background: Previous published case series have suggested an association between the onset of Bell's palsy in pregnancy and the risk of pre‐eclampsia and gestational hypertension.

Aim: To evaluate the period of onset of Bell's palsy in pregnancy and the associated risk of adverse maternal and perinatal events, including the hypertensive disorders of pregnancy.

Study design: Case series study of consecutive female patients.

Methods: Women presenting with Bell's palsy during pregnancy or the puerperium were identified by a hospital record review at five Canadian centres over 11 years. Information was abstracted about each woman's medical and obstetrical history, period of onset of Bell's palsy, and associated maternal complications, including pre‐eclampsia and gestational hypertension as well as preterm delivery and low infant birth weight (<2500>

Results: Forty‐one patients were identified. Mean onset of Bell's palsy was 35.4 weeks gestation (SD 3.9). Nine (22.0%, 95%CI 10.8–35.7) were also diagnosed with pre‐eclampsia and three (7.3%, 95%CI 1.4–17.1) with gestational hypertension, together (29.3%, 95%CI 16.5–43.9) representing nearly a five‐fold increase over the expected provincial/national average. There were three twin births. The observed rates of Caesarean (43.6%) and preterm (25.6%) delivery, as well as low infant birth weight (22.7%), were also higher than expected, although the rate of congenital anomalies (4.5%) was not.

Conclusions: The onset of Bell's palsy during pregnancy or the puerperium is probably associated with the development of the hypertensive disorders of pregnancy. Pregnant women who develop Bell's palsy should be closely monitored for hypertension or pre‐eclampsia, and managed accordingly.


In 1830, Sir Charles Bell described the association between idiopathic facial palsy (Bell's palsy) and pregnancy.1 The prevalence rate of Bell's palsy in pregnancy is estimated at 45.1 cases per 100 000 women, considerably higher than in the non‐pregnant population.2 In a systematic review, we observed that almost all cases of Bell's palsy were confined to the third trimester of pregnancy and the immediate postpartum period.3 Furthermore, there was a significantly higher rate of gestational hypertension and pre‐eclampsia (22.2%, 95%CI 12.5–36.4) among these cases, more than four times that found in the general obstetrical population.4

A limitation to previously published research into Bell's palsy in pregnancy is the absence of any systematic evaluation of important obstetrical and perinatal outcomes.3 Accordingly, these studies may have been biased toward underreporting of such events. We undertook this multi‐centre retrospective case series study with three principal objectives. First, to evaluate the timing of onset of Bell's palsy in pregnancy; second, to investigate the association between Bell's palsy and the hypertensive disorders of pregnancy; and third, to determine the prevalence of peripartum and perinatal outcomes among women who developed Bell's palsy during or immediately after pregnancy.


We reviewed the hospital charts of women diagnosed with Bell's palsy in pregnancy between 1990 and July 2001. Participants were identified through the Medical Records Departments of five Ontario hospitals: the Hamilton Health Sciences Corporation and St Joseph's Hospital, both in Hamilton; and the Sunnybrook and Women's College Health Sciences Centre, University Health Network, and Mount Sinai Hospitals, all in Toronto. A search for these charts was made using the ICD‐9CM diagnostic codes related to Bell's palsy and any concurrent pregnancy within ±12 months of the diagnosis of Bell's palsy.

From each hospital chart, we abstracted information on maternal demographics, past medical history, maternal complications during the index pregnancy, and mode of delivery. Gestational hypertension was defined as a blood pressure >140/90 mmHg after 20 weeks gestation, and pre‐eclampsia was defined as a blood pressure >140/90 mmHg, with the additional presence of at least 2+ proteinuria on dipstick or >300 mg of proteinuria over a 24‐h period. Abstracted perinatal outcomes included neonatal gestational age at birth, birth weight and the presence of any fetal anomalies detected in utero or at birth. We attempted to corroborate the chart data by contacting each patient by telephone. Perinatal outcomes and delivery information for these women were compared to rates previously described for the province of Ontario or Canada.

Using the current study data, we updated our previous systematic review3 to better estimate the rate of gestational hypertension and pre‐eclampsia among women with Bell's palsy during pregnancy or the puerperium. The rates from all studies were pooled using a random effects model,5 and the presence of significant heterogeneity for the pooled estimate was defined at a p value <0.10 id="xref-ref-6-1" class="xref-bibr" href="http://qjmed.oxfordjournals.org/content/95/6/359.full#ref-6">6

All abstracted data were entered into Microsoft Excel version 5.0c. Calculation of the pooled estimate of pre‐eclampsia and gestational hypertension was done using Meta‐Analyst 0.988.7 Permission to conduct this study was obtained from the Ethics Review Board of each participating medical centre. Permission to contact the women was obtained from their family physicians or obstetricians, and once contacted, each woman provided informed consent before being administered the telephone questionnaire.


From the five hospitals, 41 women were diagnosed with unilateral Bell's palsy between 1990 and July 2001. The hospital charts were successfully reviewed for all 41 cases, and 19 women (46%) also had their information corroborated by telephone interview. For the remaining 22 women, either their telephone number was no longer in service, or written consent to contact them could not be obtained from their family physician or obstetrician.

The pre‐pregnancy characteristics of all 41 participants are listed in Table 1. The mean maternal age was 29.0 years (SD 6.0); the majority were nulliparous (36.6%) and there were three twin pregnancies. Few had a previous history of either chronic (one woman, 2.7%) or gestational hypertension (two women, 5.4%), and none (0%) had been diagnosed with pre‐eclampsia. One had experienced Bell's palsy previously, with a full recovery before the index pregnancy (Table 1).

The mean gestational age at the onset of Bell's palsy in the index pregnancy was 35.4 weeks gestation (SD 3.9). Only one woman (2.4%) presented before 27 weeks gestation, 33 (80.5%) between 27 and 42 weeks, four (9.8%) within the first week postpartum, while for three women (7.3%) the period of onset was not defined.

Nine women (22.0%, 95%CI 10.8–35.7) were diagnosed with pre‐eclampsia and three (7.3%, 95%CI 1.4–17.1) with isolated gestational hypertension. Thus, out of 41 women with Bell's palsy, 12 (29.3%, 95%CI 16.5–43.9) developed a hypertensive disorder, nearly five times the expected rate for Ontario/Canada (Table 2).

The overall mean neonatal birth weight was 3003.3 g (SD 873.8). The corresponding rates of Caesarean delivery (43.6%), preterm birth (25.6%) and low neonatal birth weight (22.7%) were comparably higher than expected (Table 2). Of the two neonates (4.5%) born with a detectable congenital anomaly, one had Down's syndrome and the other lethal fetal hydrops.

Using the current study data, in conjunction with those 11 studies included in our previous systematic review,3 the pooled rate of combined gestational hypertension or pre‐eclampsia was 25.0% (95%CI 8.3–55.2) among 203 women with Bell's palsy in pregnancy or the puerperium.

Table 1 

Pre‐pregnancy characteristics of women with onset of Bell's palsy during the index pregnancy or puerperium

Table 2 

Maternal and perinatal outcomes among women with onset of Bell's palsy during the index pregnancy or puerperium, compared to those previously described within the general population


Of these 41 consecutive women, the majority presented with Bell's palsy during late pregnancy and the puerperium. They had an increased rate of the hypertensive disorders of pregnancy and operative delivery, while their infants experienced higher rates of preterm birth and low birth weight, compared to figures for the general population.

Study strengths and limitations

This study was probably biased by the retrospective collection of data, which was principally from the hospital charts of five large urban obstetrical centres. Since few clinicians were probably aware of the possible association between Bell's palsy and hypertension in pregnancy, it is unlikely that our estimates would have been much inflated by the presence of diagnostic suspicion bias, especially since we used objective definitions for the diagnosis of gestational hypertension and pre‐eclampsia. Although we included consecutive patients, and attempted to corroborate their chart data through telephone interviews, many could not be contacted, so some adverse perinatal events may have been missed or incorrectly recorded. In the absence of a concurrent control group, we had to rely upon national and provincial data to estimate the expected rates of adverse maternal and perinatal outcomes within the five participating centres. Such comparisons cannot account for possible differences between the women studied herein and those previously selected for large epidemiological studies. Finally, the presence of statistical heterogeneity for the pool estimate of pre‐eclampsia and gestational hypertension could be explained by the fact that previous investigators did not systematically assess for these events, or define them using standard criteria.3

Evidence for an association between Bell's palsy and pre‐eclampsia

Our results suggest that the vast majority of women who develop Bell's palsy in pregnancy had no known risk factors before pregnancy, including diabetes mellitus or chronic hypertension. As with previously published data, our findings support the hypothesis of an association between Bell's palsy and pre‐eclampsia.3 First, the observed rate of pre‐eclampsia was approximately five times higher than expected. Second, both disorders appeared late in pregnancy, and very rarely before the second trimester. Third, more women with Bell's palsy developed pre‐eclampsia (22%) than gestational hypertension (7.3%), suggesting that Bell's palsy and pre‐eclampsia may share a common pathway in their manifestation and pathogenesis, as outlined below.

Women in their third trimester of pregnancy may be predisposed to Bell's palsy due to the increase in maternal extracellular fluid volume during this period.12 Other nerve compression syndromes, including carpal tunnel syndrome,13 are also seen more commonly in the latter part of pregnancy.14 An increase in perineural oedema, resulting in facial nerve impingement, may form the underlying basis for facial nerve palsy.15 Pre‐eclampsia often manifests with considerable oedema within both subcutaneous and nervous system tissues,16 probably creating a neuro‐compressive effect. A second possible explanation may be the presence of a hypercoagulable state associated with pre‐eclampsia, resulting in thrombosis of the vasa nervorum, thereby leading to nerve ischemia and paralysis.15 Since the aetiology of Bell's palsy remains unknown, but is probably multifactorial,17 these and other mechanisms may provide insight into the treatment and recovery of ‘idiopathic’ facial palsy in pregnancy.

Clinical and research recommendations

Regardless of its aetiology, the notion that Bell's palsy in pregnancy may be associated with impending pre‐eclampsia cannot be overlooked. For these women, we recommend heightening maternal and fetal surveillance for the remainder of pregnancy. Although our data do not permit us to comment on the recovery of Bell's palsy after delivery, others have observed nearly 100% recovery in women with incomplete palsy, but only a 52% satisfactory outcome in the presence of a complete facial paralysis.18 Thus, research is needed to better characterize the association between Bell's palsy and pre‐eclampsia, and the relative rate of recovery of facial palsy in such cases. Investigators might also consider whether certain drugs used in the treatment of pre‐eclampsia (e.g. magnesium sulphate) can worsen the recovery of Bell's palsy,19 as well as the benefit of other therapies, including corticosteroids.20



Thursday, November 4, 2010

MMR vaccination and autism

News & RSS | Hitting the Headlines Archive | Article


06 Feb 2008

MMR vaccination and autism

There is no link between the MMR vaccination and autism, reported eight newspapers (5 February 2008). The newspaper reports were based on a well-conducted case-control study and were generally accurate. The study findings are likely to be reliable.

  • On 5 February 2008, eight newspapers (1-8) reported that there is no link between the MMR vaccine and autism.

  • The reports were based on a study published in the Archives of Disease in Childhood (9). The study compared 98 vaccinated children aged 10-12 years with autism spectrum disorders (ASD) to two control groups (also vaccinated) comprising 52 children with special educational needs but no ASD and 90 typically developing children within the same geographical area. There was no evidence of a differential response to measles virus or the measles component of the MMR between children with ASD, with or without regression, and controls who had either one or two doses of MMR.

  • Six of the papers accurately report the key findings from the study and in two there is no reporting of the study results (7-8). The study appears well conducted and the conclusions are likely to be reliable. The findings of the study are in line with previous epidemiological studies showing no association between MMR vaccination and the development of autism.

Evaluation of the evidence base for measles vaccination and antibody response in autism spectrum disorders

Where does the evidence come from?

The research was conducted by Professor G Baird and colleagues from Guy's & St Thomas' NHS Foundation Trust in London and various hospitals and research institutes in the UK. The study was funded by the Department of Health, the Wellcome Trust, the National Alliance for Autism Research (NAAR) and Remedi.

What were the authors' objectives?

To test the hypothesis that measles vaccination was involved in the pathogenesis of autism spectrum disorders (ASD) as evidenced by signs of a persistent measles infection or abnormally persistent immune response in children with ASD who had been vaccinated against MMR compared with controls.

What was the nature of the evidence?

A community based case-control study was conducted of 240 children aged 10-12 years. Children with a diagnosis of ASD were identified among a cohort of 56,946 children from 12 districts in the South Thames Region of the UK. Controls with a statement of special educational needs (SEN) but no ASD diagnosis were identified from the same cohort. A second control group comprised typically developing children born at the same time and in the same area as the ASD cases. Children whose blood samples showed that they had received at least one MMR vaccination were eligible for the study.

How did participants differ on their level of exposure to the factor of interest?

A total of 235 children had received the first MMR vaccination: 98 with ASD, 52 SEN controls, and 85 typically developing controls. Stage 2 MMR vaccination was received by 106 children: 35 children with ASD, 18 SEN controls and 53 typically developing controls. Five children with no evidence of at least one MMR vaccination were excluded from the analysis. The particular factors of interest were the detection of the measles genome or measles antibody concentrations and whether these differed between the ASD group and the control groups. An additional factor of interest was whether the presence of bowel symptoms (enterocolitis) differed between the groups.

What were the findings?

No difference was detected in the distribution of measles antibody or in measles virus in ASD cases and controls whether the children had received the first, second or both MMR vaccinations. When the analysis was restricted to ASD cases with a history of regression there remained no difference between the groups. Only one child, who did not have ASD or regression, had symptoms of possible enterocolitis.

What were the authors' conclusions?

There is no association between measles vaccination and ASD. In this cohort children were less likely to receive the second MMR vaccination after diagnosis of a developmental problem.

How reliable are the conclusions?

The research was a well-conducted case-control study, the largest of its type to be undertaken, and the conclusions are likely to be reliable. ASD cases and SEN controls were located by screening a large cohort of children likely to be representative of the general population. The selection of the patients, and allocation into study groups, was based on the use of standardised tools for the diagnostic assessment of autism. Rigorous methods were used to assess both exposure to MMR vaccine and the presence of measles virus or antibodies to the virus. The typically developing control group was not obtained from a randomised selection process and through inviting participation in the study it is possible that a biased group elected to participate. The findings of the study are in line with previous epidemiological studies showing no association between MMR vaccination and the development of ASD.

Systematic reviews

Information staff at CRD searched for systematic reviews relevant to this topic. Systematic reviews are valuable sources of evidence as they locate, appraise and synthesize all available evidence on a particular topic.

There was one related systematic review identified on the Cochrane Database of Systematic Reviews (CDSR) (10) and two on the Database of Abstracts of Reviews of Effects (DARE) (11,12).

References and resources

1. The research that 'disproves MMR jab link to autism'. The Daily Mail, 5 February 2008, p4.

2. MMR and autism link is dismissed. The Times, 5 February 2008, p18.

3. MMR vaccine does not cause autism, says study. The Daily Telegraph, 5 February 2008, p7.

4. MMR links to autism dismissed by huge study. The Guardian, 5 February 2008, p1.

5. No link between the MMR jab and autism. Daily Mirror, 5 February 2008, p26.

6. Parents' anger over new 'evidence' that the MMR jab is safe. Daily Express, 5 February 2008, p17.

7. MMR jab given OK. The Sun, 5 February 2008, p21.

8. Autism 'is not linked to MMR'. The Independent, 5 February 2008, p13.

9. Baird G, Pickles A, Simonoff E [et al.]. Measles vaccination and antibody response in autism spectrum disorders. Archives of Disease in Childhood. Online publication February 5 2008 doi:10.1136/adc.2007.122937.

10. Demicheli V, Jefferson T, Rivetti A, Price D. Vaccines for measles, mumps and rubella in children. The Cochrane Database of Systematic Reviews 2005, Issue 4. Art. No.: CD004407. DOI: 10.1002/14651858.CD004407.pub2.

11. Jefferson T, Price D, Demicheli V, Bianco E, European Research Program for Improved Vaccine Safety. Unintended events following immunization with MMR: a systematic review. Vaccine 2003;21(25-26):3954-3960. [DARE Abstract]

12. Wilson K, Mills E, Ross C, McGowan J, Jadad A. Association of autistic spectrum disorder and the measles, mumps, and rubella vaccine: a systematic review of current epidemiological evidence. Archives of Pediatrics and Adolescent Medicine 2003;157(7):628-34. [DARE Abstract]

Consumer information

NHS - MMR the facts

Health Education Board for Scotland (HEBS) - MMR Information Centre

National Autistic Society

Previous Hitting the Headlines summaries on this topic

MMR not linked to autism: new study. Hitting the Headlines archive, 7 July 2006.

'Lingering fears of MMR-autism link dispelled'. Hitting the Headlines archive, 3 March 2005.

'Doctor's doubt on all-clear for MMR and autism link'. Hitting the Headlines archive, 11 October 2004.

MMR study finds no link with autism. Hitting the Headlines archive, 10 September 2004.

Bowel virus, autism and MMR. Hitting the Headlines archive, 13 January 2004.

'New research supports concern over MMR jab'. Hitting the Headlines archive, 16 December 2003.

Can mercury in jabs double the risk of autism? Hitting the Headlines archive, 19 November 2003.

The MMR vaccine and autism. Hitting the Headlines archive, 21 May 2003.

New study on MMR and autism. Hitting the Headlines archive, 7 November 2002.

'MMR may be linked to autism'. Hitting the Headlines archive, 9 August 2002.

Study finds no evidence of MMR and autism link. Hitting the Headlines archive, 12 &13 June 2002

What is the evidence for and against the MMR vaccine? Part 1. Hitting the Headlines archive, 7 February 2002.

What is the evidence for and against the MMR vaccine? Part 2. Hitting the Headlines archive, 7 February 2002.

Misreporting Measles Research. Hitting the Headlines archive, 6 February 2002.

The MMR vaccine debate. Hitting the Headlines archive, 24 September 2001.

Biggest study clears MMR jab. Hitting the Headlines archive, 12 January 2001.

Further information about Hitting the Headlines

Further information about Hitting the Headlines, together with selected relevant links, can be found at http://www.library.nhs.uk/hth/.

Centre for Reviews and Dissemination

Publication Date:
06 Feb 2008

Wednesday, June 23, 2010

Diagnosis and Treatment of Premenstrual Dysphoric Disorder

Diagnosis and Treatment of Premenstrual Dysphoric Disorder


Creighton University School of Medicine, Omaha, Nebraska

Am Fam Physician.�2002�Oct�1;66(7):1239-1249.

� Patient Information Handout

From 2 to 10 percent of women of reproductive age have severe distress and dysfunction caused by premenstrual dysphoric disorder, a severe form of premenstrual syndrome. Current research implicates mechanisms of serotonin as relevant to etiology and treatment. Patients with mild to moderate symptoms of premenstrual syndrome may benefit from nonpharmacologic interventions such as education about the disorder, lifestyle changes, and nutritional adjustments. However, patients with premenstrual dysphoric disorder and those who fail to respond to more conservative measures may also require pharmacologic management, typically beginning with a selective serotonin reuptake inhibitor. This drug class seems to reduce emotional, cognitive-behavioral, and physical symptoms, and improve psychosocial functioning. Serotoninergic antidepressants such as fluoxetine, citalopram, sertraline, and clomipramine are effective when used intermittently during the luteal phase of the menstrual cycle. Treatment strategies specific to the luteal phase may reduce cost, long-term side effects, and risk of discontinuation syndrome. Patients who do not respond to a serotoninergic antidepressant may be treated with another selective serotonin reuptake inhibitor. Low-dose alprazolam, administered intermittently during the luteal phase, may be considered as a second-line treatment. A therapeutic trial with a gonadotropin-releasing hormone agonist or danazol may be considered when other treatments are ineffective. However, the risk of serious side effects and the cost of these medications limit their use to short periods.

Millions of women of reproductive age have recurrent emotional, cognitive, and physical symptoms related to their menstrual cycles. These symptoms often recur discretely during the luteal phase of the menstrual cycle and may significantly interfere with social, occupational, and sexual functioning.

Premenstrual dysphoric disorder (PMDD), a severe form of premenstrual syndrome (PMS), is diagnosed by the pattern of symptoms. According to a report by the Committee on Gynecologic Practice of the American College of Obstetricians and Gynecologists,1 up to 80 percent of women of reproductive age have physical changes with menstruation; 20 to 40 percent of them experience symptoms of PMS, while 2 to 10 percent report severe disruption of their daily activities. Menstruation-related physical discomfort, such as dysmenorrhea, may begin with menarche. Often this condition is superseded by PMS in late adolescence or the early 20s. These syndromes generally remain stable over time.


In the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV), PMDD is classified as “depressive disorder not otherwise specified” and emphasizes emotional and cognitive-behavioral symptoms.2� At least five of the 11 specified symptoms must be present for a diagnosis of PMDD (Table 1).2 These symptoms should be limited to the luteal phase and should not represent amplification of preexisting depression, anxiety, or personality disorder. In addition, they must be confirmed prospectively by daily rating for at least two consecutive menstrual cycles. A symptom-free period during the follicular phase of the menstrual cycle is essential in differentiating PMDD from preexisting anxiety and mood disorders.
Research Criteria for Premenstrual Dysphoric Disorder

A. In most menstrual cycles during the past year, five (or more) of the following symptoms were present for most of the time during the last week of the luteal phase, began to remit within a few days after the onset of the follicular phase, and were absent in the week postmenses, with at least one of the symptoms being either (1), (2), (3), or (4):


Markedly depressed mood, feelings of hopelessness, or self-deprecating thoughts

Marked anxiety, tension, feelings of being “keyed up” or “on edge”

Marked affective lability (e.g., feeling suddenly sad or tearful or increased sensitivity to rejection)

Persistent and marked anger or irritability or increased interpersonal conflicts

Decreased interest in usual activities (e.g., work, school, friends, hobbies)

Subjective sense of difficulty in concentrating

Lethargy, easy fatigability, or marked lack of energy

Marked change in appetite, overeating, or specific food cravings

Hypersomnia or insomnia

A subjective sense of being overwhelmed or out of control

Other physical symptoms, such as breast tenderness or swelling, headaches, joint or muscle pain, a sensation of “bloating,” or weight gain

B. The disturbance markedly interferes with work or school or with usual social activities and relationships 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 major depressive disorder, panic disorder, dysthymic disorder, or a personality disorder (although it may be superimposed on any of these disorders).

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

note:In menstruating females, the luteal phase corresponds to the period between ovulation and the onset of menses, and the follicular phase begins with menses. In nonmenstruating females (e.g., those who have had a hysterectomy), the timing of luteal and follicular phases may require measurement of circulating reproductive hormones.

Reprinted with permission from the American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, D.C.: American Psychiatric Association, 1994:717–8. Copyright 1994.

Researchers have developed a reliable and valid self-reporting scale called the Daily Symptom Report (see patient information handout).3 The report consists of 17 common PMS symptoms, including 11 symptoms from the DSM-IV PMDD diagnostic criteria. Patients rate each symptom on a five-point scale, from zero (none) to 4 (severe). The scale provides guidance for scoring the severity of each symptom and may be used in the office setting by primary care physicians for diagnosis and assessment of PMDD.


Currently, there is no consensus on the cause of PMDD. Biologic, psychologic, environmental and social factors all seem to play a part. Genetic factors are also pertinent: 70 percent of women whose mothers have been affected by PMS have PMS themselves, compared with 37 percent of women whose mothers have not been affected.4 There is a 93 percent concordance rate in monozygotic twins, compared with a rate of 44 percent in dizygotic twins.4 Genetic influences mediated phenotypically through neurotransmitters and neuroreceptors seem to play a significant role in the etiology.

Features of PMDD and depressive disorders—specifically atypical depression—overlap considerably. Symptoms of atypical depression (i.e., depressed mood, interpersonal rejection hypersensitivity, carbohydrate craving, and hypersomnia) are similar to those of PMDD. Thirty to 76 percent of women diagnosed with PMDD have a lifetime history of depression,5 compared with 15 percent of women of a similar age without PMDD. A family history of depression is common in women diagnosed with moderate to severe PMS.6 There is significant comorbidity between depression and PMDD. Despite this relationship, many patients with PMDD do not have depressive symptoms; therefore, PMDD should not be considered as simply a variant of depressive disorder.7

The effectiveness of selective serotonin reuptake inhibitors (SSRIs), administered only during the luteal phase of the menstrual cycle,8–14 highlights the difference between PMDD and depressive disorder. Acute treatment with SSRIs increases synaptic serotonin without the down-regulation of serotonin receptors needed for improvement in overt depression. This finding suggests that PMDD is possibly caused by altered sensitivity in the serotoninergic system in response to phasic fluctuations in female gonadal hormone. Other studies also favor the serotonin theory as a cause of PMDD. In particular, the efficacy of l-tryptophan,15 a precursor of serotonin, and of pyridoxine,16 which serves as a cofactor in the conversion of tryptophan into serotonin, also favors serotonin deficiency as a cause of PMDD. Carbohydrate craving, often a symptom of PMDD, is also mediated through serotonin deficiency.

Because PMDD only affects women of reproductive age, it is reasonable to assume that female gonadal hormones play a causative role, possibly mediated through alteration of serotoninergic activity in the brain. Estrogen and progesterone seem to modulate levels of monoamines, including serotonin. Eliminating the effect of ovarian gonadal hormones through the use of a gonadotropin-releasing hormone (GnRH) agonist relieves PMDD symptoms.17 Subsequent administration of estrogen and progesterone causes symptoms to return in women with PMS but not in those without PMS symptoms.18


The goals of treatment in patients with PMDD are (1) symptom reduction and (2) improvement in social and occupational functioning, leading to an enhanced quality of life. Available treatment options are summarized in Tables 2 through 6.


Lifestyle changes may be valuable in patients with mildly severe symptoms and benefit their overall health. Aerobic exercise and dietary changes often reduce premenstrual symptoms.19,20 Decreasing caffeine intake can abate anxiety and irritability, and reducing sodium decreases edema and bloating. Many patients prefer to try lifestyle changes and/or nutritional supplements as a first step in the treatment of PMDD.


Many of the nutritional supplements described in Table 24,15,16,19–22 have proven efficacy. A meta-analysis16 of nine randomized, placebo-controlled trials was conducted to ascertain the effectiveness of vitamin B6 in PMS management. The researchers concluded that vitamin B6, in dosages of up to 100 mg per day, is likely to benefit patients with premenstrual symptoms and premenstrual depression. In another study,21 research literature (from January 1967 to September 1999) was reviewed to evaluate the effectiveness of calcium carbonate in patients with PMS. The reviewers concluded that calcium supplementation in a dosage of 1,200 to 1,600 mg per day is a treatment option in women with PMS. Calcium supplementation (using Tums E-X) was found to reduce core premenstrual symptoms by 48 percent in 466 patients.22 Vitamin E, an antioxidant, seems to reduce the affective and physical symptoms of PMS.20 Tryptophan,15 a substrate for serotonin, may also benefit some patients.15
Treatment Approaches to PMDD

Lifestyle changes

Regular, frequent, small balanced meals rich in complex carbohydrates and low in salt, fat, and caffeine19,20

Regular exercise19,20

Smoking cessation20

Alcohol restriction20

Regular sleep20

Nutritional supplements

Vitamin B6, up to 100 mg per day16

Vitamin E, up to 600 IU per day20

Calcium carbonate, 1,200 to 1,600 mg per day21,22

Magnesium, up to 500 mg per day20

Tryptophan, up to 6 g per day15

Nonpharmacologic treatments

Stress reduction and management20

Anger management4

Self-help support group20

Individual and couples therapy20

Cognitive-behavioral therapy23

Patient education20 about the cause, diagnosis, and treatment of PMS/PMDD

Light therapy20 with 10,000 Lx cool-white fluorescent light

PMDD = premenstrual dysphoric disorder; PMS = premenstrual syndrome.

Information from references 4,15,16, and 19 through 23.


Almost invariably, psychosocial stressors should be addressed, either as a cause or a result of PMDD. Psychosocial stressors are known to alter brain neurochemistry and stress-related hormonal activity. Stress reduction, assertiveness training, and anger management can reduce symptoms and interpersonal conflicts. Women with negative views of themselves and the future caused or exacerbated by PMDD may benefit from cognitive-behavioral therapy.23 This kind of therapy can enhance self-esteem and interpersonal effectiveness, as well as reduce other symptoms.23 Educating patients and their families about the disorder can promote understanding of it and reduce conflict, stress, and symptoms.20


A recent study24� reviewed efficacy and safety data on herbal supplements marketed for women. The author concluded that two herbal products, evening primrose oil and chaste tree berry, have been effective in treating PMS (Table 3).24–26 Other researchers25 have arrived at variable conclusions about the efficacy of evening primrose oil. It is thought to provide the gamma-linolenic acid required for synthesis of prostaglandin E1,24 one of the anti-inflammatory prostaglandins. Chaste tree berry may reduce prolactin levels,24,25 thereby reducing symptoms of breast engorgement. These herbal therapies have not been approved by the U.S. Food and Drug Administration (FDA) for use in PMDD, and their safety in pregnancy and lactation has not been established. Moreover, manufacturing standards for herbal products are not uniform.
Herbal Therapies for PMDD
Herbal product Dosage Use recommendation Comments

Evening primrose oil24,25

500 mg per day to 1,000 mg three times per day

Days 17 through 28 of menstrual cycle

Most-studied of all herbs used in treatment of PMS

May provide a precursor for prostaglandin synthesis

Benefits breast tenderness

Safety data in pregnancy and lactation lacking

Not approved for this use by the FDA

Chaste tree berry24–26

30 to 40 mg per day

Days 17 through 28 of menstrual cycle

May benefit breast symptoms

Inhibits prolactin production

Safety data lacking

Not approved for this use by the FDA

PMDD = premenstrual dysphoric disorder; PMS = premenstrual syndrome; FDA = U.S. Food and Drug Administration.

Information from references 24 through 26.


Antidepressant and Anxiolytic Medications

The serotoninergic antidepressants are the first-line treatment of choice for severe PMDD (Table 4).8–14,27–37 Fluoxetine, in a dosage of 20 mg per day, has been shown to be superior to placebo, whether used only during the luteal phase12 or throughout the full menstrual cycle.27–29 In a review29 of seven controlled and four open-label clinical trials of fluoxetine, symptoms were significantly reduced in patients with PMDD.
Pharmacologic Interventions: Antidepressant and Anxiolytic Medications
Agents Dosage Use recommendation Comments



10 to 30 mgper day

Full cycle or luteal phase only

Benefits physical, cognitive, and emotional symptoms

Administration during luteal phase

Luteal-phase use is superior to continuous treatment

Not approved by FDA for this use


20 mg per day

Full cycle or luteal phase only

Significant reduction of all symptoms

Decreased libido or delayed orgasm is most common side effect in long-term, continuous use

Approved by FDA for this use


10 to 30 mgper day

Full cycle

Benefits all symptoms

Transient GI and sexual side effects

Superior to maprotiline

Not approved by FDA for this use


50 to 150 mg per day

Full cycle or luteal phase only

Benefits all symptoms

Transient GI and sexual side effects

Approved by FDA for this use

Other serotoninergic antidepressants


25 to 75 mgper day

Full cycle or luteal phase only

Benefits all symptoms

Anticholinergic and sexual side effects

Not approved by FDA for this use



0.375 to 1.5 mg per day

Luteal phase

Interrupted use during the luteal phase can reduce the risk of drug dependence

Use only if SSRIs are ineffective

Not approved by FDA for this use

SSRIs = selective serotonin reuptake inhibitors; FDA = U.S. Food and Drug Administration; GI = gastrointestinal.

Information from references 8 through 14, and 27 through 37.

In one placebo-controlled study,30 paroxetine in a dosage of 10 to 30 mg per day improved mood and physical symptoms in patients with PMDD. Paroxetine was more effective than the noradrenaline reuptake inhibitor maprotiline.30 Sertraline in a dosage of 50 to 150 mg per day was superior to placebo whether used during the full menstrual cycle31–33 or only during the luteal phase.8–10,14 Citalopram in a dosage of 10 to 30 mg per day was effective in one randomized, placebo-controlled trial.13 Interestingly, intermittent administration of citalopram during the luteal phase was found to be superior to continuous treatment. Clomipramine, a serotoninergic tricyclic antidepressant that affects the noradrenergic system, in a dosage of 25 to 75 mg per day used during the full cycle34 or intermittently during the luteal phase,11 significantly reduced the total symptom complex of PMDD.

In a recent meta-analysis35 of 15 randomized, placebo-controlled studies of the efficacy of SSRIs in PMDD, it was concluded that SSRIs are an effective and safe first-line therapy and that there is no significant difference in symptom reduction between continuous and intermittent dosing. Because fluoxetine, citalopram, clomipramine, and sertraline were effective if administered during the luteal phase only, these drugs may be used as first-line therapy and taken intermittently only during the luteal phase. Such an approach can reduce the risk of long-term side effects (e.g., weight gain), minimize discontinuation syndrome, and reduce the cost of care. SSRIs benefit the total symptom complex of PMDD, not only the mood-related symptoms. It should also be noted that fluoxetine and sertraline are the only two SSRIs with FDA approval for use in the treatment of PMDD.

Alprazolam, a high-potency benzodiazepine with mood-enhancing and anxiolytic effects, has been shown to be somewhat effective in patients with PMS.28,36,37 Because of the potential for drug dependence, alprazolam should be considered a second-line drug and used only if SSRIs fail to achieve an optimal response. Therapy should be limited to the luteal phase, and the agent should be given in low dosages—0.375 to 1.5 mg per day. The risk of drug dependence with alprazolam can be minimized by administering it only during the luteal phase of the menstrual cycle in patients without a history of substance abuse.

Hormonal Therapies

It has been shown that by inducing anovulation and amenorrhea, GnRH agonists, leuprolide, histrelin, and goserelin provide significant relief of symptoms in patients without comorbid depression.38–40 However, these medications can induce menopausal symptoms such as hot flushes, vaginal dryness, fatigue, irritability, cardiac problems, and osteopenia. In women with a history of PMDD, treatment of induced menopause with estrogen39 or estrogen plus progestational agents18 can induce recurrent symptoms of PMDD. This finding supports the theory of an etiologic role for female gonadal hormones in PMDD.

Danazol (Danocrine), a weak androgen prescribed for patients with endometriosis, fibrocystic breast disease, and hereditary angioneurotic edema, is sometimes used to treat PMDD. The typical dosage is 100 mg twice a day. Such treatment can reduce symptoms but may result in anovulation and masculinization, either of which may limit regular use.41 Because of the potential for serious side effects and significant costs, GnRH agonists and danazol should be tried as a last resort. These medications must be initiated during menstruation to prevent teratogenicity if there is an unintended pregnancy.

Although oral contraceptive pills (OCPs) suppress ovulation, they are not reported to be consistently effective in the treatment of PMDD (perhaps because the studies had variable samples). OCPs may not suffice if mood symptoms are prominent and, in some patients, these drugs may worsen dysphoria (a known side effect of some birth control pills) in many women without PMDD.

Efficacy studies of progesterone have shown limited benefits. One study42 found progesterone to be superior to placebo; however, another study43� reported efficacy equal to or less than that of placebo. Currently, ovarian gonadal hormones are thought to be of limited usefulness in the treatment of PMDD, and none of the drugs has FDA approval for this indication (Table 5).18,20,38–43
Hormonal Therapies for PMDD
Drug Dosage Use recommendation Comments

Leuprolide depot38,40

3.75 mg IM per month

Up to six cycles

Pregnancy category X

Significant relief from symptoms but can induce menopausal syndrome

Leuprolide depot with ovarian hormone supplements18

3.75 mg IM per month with estrogen and progesterone

Can exceed six cycles

Less likely to induce menopause; PMDD symptoms may return, making this combination less effective

Goserelin with estrogen supplementation39

3.6 mg SC every 28 days with estrogen

Can exceed six cycles

Less likely to induce menopause; PMDD symptoms may return, making this combination less effective

Pregnancy category X

Use nonhormonal contraception during therapy and for 12 weeks after discontinuation of drug or until menses resume


100 mg twice a day

Up to six cycles

May cause masculinization from weak androgenic properties

Pregnancy category X


OCPs with varying amounts of estrogen and progesterone, once a day

Full cycle

Variable response; may not benefit patients with significant mood symptoms; in some patients, may make mood symptoms worse


Vaginal suppositories, 200 to 400 mg per day

Not recommended for this use

Questionable efficacy

PMDD = premenstrual dysphoric disorder; IM = intramuscularly; SC = subcutaneously; OCPs = oral contraceptive pills.

Information from references 18,20, and 38 through 43.

Miscellaneous Pharmacologic Interventions

In a double-blind, placebo-controlled, crossover study,44 spironolactone in a dosage of 100 mg per day was more effective than placebo in reducing irritability, depression, somatic symptoms, feelings of swelling, breast tenderness, and craving for sweets. Bromocriptine in a dosage of up to 2.5 mg three times per day may be beneficial in patients with cyclic mastalgia,4,20 although in one study45 it was not found to be effective. Ibuprofen, in a dosage of up to 1,000 mg per day, can reduce breast pain, headaches, back pain, and other pain symptoms,20� but seems to have limited effect on mood symptoms (Table 6).4,20,44,45
Miscellaneous Pharmacologic Interventions for PMDD
Agents Dosage Use recommendation Comments



100 mg per day

Luteal phase

Aldosterone antagonist

Potassium-sparing diuretic

Could improve physical and psychologic symptoms

Dopamine agonist


Up to 2.5 mg three times per day

Days 10 through 26 of menstrual cycle

May relieve cyclic mastalgia; evaluate hepatic and renal functions before initiation



500 to 1,000 mg per day

Days 17 through 28 of menstrual cycle

Take with food May relieve mastalgia

PMDD = premenstrual dysphoric disorder; NSAIDs = nonsteroidal anti-inflammatory drugs.

Information from references 4,20,44, and 45.

Other Medical Interventions

Historically, surgical and radiation oophorectomies have been used to treat severe PMS, but these modalities have no role in the current management of PMDD.

Evidenced-based efficacy ratings of currently available treatments for PMS and PMDD are described in Table 7,8–16,19–25,28–39,41–45 while an algorithm for the management of these conditions is outlined in Figure 1.
Efficacy Rating of Current Treatments for PMS/PMDD
Recommended treatment Efficacy in PMS/PMDD Efficacy rating* Comments/evidence

Lifestyle changes19,20



Health benefits without risks

Vitamin B616



Dosage > 100 mg per day may cause peripheral neuropathy

Vitamin E20



Antioxidant without significant risk

Calcium carbonate21,22



Placebo-controlled study supports benefits in moderate to severe PMS




Supported by a placebo-controlled study

Cognitive-behavioral therapy23



Benefits documented; not many studies



Herbal therapies24,25



Safety in pregnancy and lactation not documented; not FDA-approved

Selective serotonin reuptake inhibitors8–10,12–14,29–33,35

Nonresponsive PMS or PMDD


Well-designed, randomized, placebo-controlled studies and metaanalyses




Anticholinergic side effects




Low-dose, luteal phase treatment; long-term use may cause tolerance

GnRH agonists or danazol18,38,39,41,42



Menopausal syndrome/masculinization/cost limit its use

Spironolactone, bromocriptine, or ibuprofen41,44,45



Symptom-focused efficacy; spironolactone efficacy supported by double-blind study

Oral contraceptives or progesterone42,43



Anecdotal efficacy or not consistently effective

Surgical or radiation oophorectomy



Not recommended

PMS = premenstrual syndrome; PMDD = premenstrual dysphoric disorder; FDA = U.S. Food and Drug Administration; GnRH = gonadotropin-releasing hormone.

*—Efficacy rating key: A = first line; B = second line; C = third line; D = symptomatic efficacy; E = efficacy anecdotal or not consistently effective; F = not recommended; G = general or adjunctive treatments.

Information from references 8 through 16,19 through 25,28 through 39, an d41 through 45.

Management of PMS/PMDD


Algorithm for the management of PMS/PMDD. (PMS = premenstrual syndrome; PMDD = premenstrual dysphoric disorder; SSRI = selective serotonin reuptake inhibitor; GnRH = gonadotropin-releasing hormone.)

The Authors

SUBHASH C. BHATIA, M.D., is chief of the Mental Health and Behavioral Science Department at the Department of Veterans Affairs, Nebraska–Western Iowa Health Care System, Omaha. He is also professor of psychiatry at Creighton University School of Medicine and clinical associate professor at the University of Nebraska College of Medicine, both in Omaha. A medical graduate of Panjab University, Chandigarh, India, Dr. Bhatia received a graduate degree from the Postgraduate Institute of Medical Education and Research, also in Chandigarh, and completed a residency in psychiatry at Creighton University. Dr. Bhatia is board-certified in psychiatry, geriatric psychiatry, addiction psychiatry, and forensic psychiatry.

SHASHI K. BHATIA, M.D., is director of child and adolescent residency education and training at Creighton University School of Medicine, where she is also associate professor of psychiatry, child and adolescent psychiatry, and pediatrics. In addition, she serves as clinical associate professor at the University of Nebraska College of Medicine. A medical graduate of Panjab University, Dr. Bhatia completed a residency in obstetrics and gynecology at the Postgraduate Institute of Medical Education and Research and a residency in psychiatry and child psychiatry at Creighton University. Dr. Bhatia is board-certified in psychiatry, child and adolescent psychiatry, addiction psychiatry, and forensic psychiatry.

Address correspondence to Subhash C. Bhatia, M.D., Chief, Mental Health and Behavioral Science Department, Department of Veterans Affairs, Nebraska–Western Iowa Health Care System, 4101 Woolworth Ave., Omaha, NE 68105 (e-mail: subhash.bhatia@med.va.gov). Reprints are not available from the authors.

The authors thank Daniel Richard Wilson, M.D., Ph.D., Professor and Chair, Creighton University School of Medicine, Department of Psychiatry, for constructive suggestions for the manuscript.

Dr. Shashi Bhatia is a member of the speakers bureaus of Abbot Laboratories and Forest Pharmaceutical, Inc. Dr. Subhash Bhatia is a member of the speakers bureaus for Eli Lilly and Co., Pfizer US Pharmaceutical Group, and Forest Pharmaceutical, Inc. Sources of funding: none reported.


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Firman Abdullah Bung

drFirman Abdullah SpOG / ObGyn

drFirman Abdullah SpOG / ObGyn


Dr Firman Abdullah SpOG/ OBGYN, Bukittinggi, Sumatera Barat ,Indonesia

Dr Firman Abdullah SpOG/ OBGYN,                              Bukittinggi, Sumatera Barat ,Indonesia

Bukittinggi , Sumatera Barat , Indonesia

Bukittinggi , Sumatera Barat  , Indonesia
Balaikota Bukittinggi

dr Firman Abdullah SpOG / OBGYN

dr Firman Abdullah SpOG / OBGYN

Ngarai Sianok ,Bukittinggi, Sumatera Barat.Indonesia

Ngarai Sianok ,Bukittinggi, Sumatera Barat.Indonesia

Brevet in Specialist Obstetric's & Gynecologist 1998

Brevet in Specialist Obstetric's & Gynecologist 1998
dr Firman Abdullah SpOG/ObGyn

Dokter Spesialis Kebidanan dan Penyakit Kandungan . ( Obstetric's and Gynaecologist ) . Jl.Bahder Johan no.227,Depan pasar pagi ,Tembok .Bukittinggi 26124 ,HP:0812 660 1614. West Sumatra,Indonesia

Sikuai Beach ,West Sumatra ,Indonesia

Sikuai Beach ,West Sumatra ,Indonesia

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