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Premenstrual Dysphoric Disorder (PMDD): Pathogenesis, Symptoms & Treatment

Premenstrual dysphoric disorder is a severe form of premenstrual syndrome which often affects 3% – 8% of women. It`s a diagnosis associated with the luteal phase of the menstrual cycle. The disorder is a premenstrual syndrome that is so severe that it can be debilitating due to physical, mental or emotional symptoms. Treatment is recommended because it interferes with the patient`s ability to function in his/her social and professional life.

Premenstrual Dysphoric Disorder

The cardinal symptom that persists between ovulation and menstruation, and disappears a few after days after the onset of singing is irritability. Anxiety, anger and depression can also occur.

Changing your lifestyle, like regular exercise and a well-balanced diet, may improve the symptoms. There is evidence that vitamin B6 in doses up to 100 mg can relieve TSH symptoms. Some serotonin reuptake inhibitors can also ameliorate. The US Food and Drug Association approved 4 drugs for this disorder: fluoxetine (Prozac), sertraline, paroxetine and escitalopram oxalate.

Pathogenesis & Causes

The main theories explaining the pathophysiology of this disorder are:

  • Ovarian hormone hypothesis.
  • Serotonin hypothesis.
  • Psychosocial hypothesis.
  • Social and cognitive learning theory.
  • Socio-cultural theory.

Ovarian Hormone Hypothesis

It assumes that the disease is caused by an imbalance between the estrogen and progesterone ratio of relatively progesterone deficiency. Based on this theory, several women with premenstrual syndrome were treated. However, recent studies of estrogen and progesterone levels among women with premenstrual syndrome were inconclusive due to methodological difficulties. The current consensus seems to be that normal fluctuations of gonadal hormones trigger central clinical-biologic events associated with premenstrual syndrome in predisposed women.

Read more on Premenstrual Syndrome: Causes & Symptoms, Risk Factors & Investigations!

Serotonin Hypothesis

It hypothesized that the function of ovarian hormones, and not their imbalance, is the clinical trigger for the biochemical events associated with the central nervous system and other target tissues. The disorder shares many of the phenomenological features of depression and anxiety that have been linked to serotoninergic deregulation. Study data show that 5-hydroxytryptamine may be important in the etiology of the disease. Low serotoninergic activity in women is altered premenstrual. The administration of serotonin induces a change in affectivity. Transient agents lowering serotonin activity have been associated with behavioral changes, including irritability and social isolation.

Psychosocial Hypothesis

It hypothesizes that premenstrual dysphoric disorder is a consequence of manifesting unconscious conflicts of a woman on femininity and maternity. Psychoanalysts suggest that premenstrual physical changes remind women that they are not pregnant and thus do not fulfill their traditional female role.

Social & Cognitive Learning Hypothesis

It hypothesizes that the onset of menstruation is a psychosocial aversive event for the susceptible woman to the disorder. Moreover, these women may have negative and extreme thoughts that increase the aversion of premenstrual symptoms. Then it develops coping strategies, such as affective lability, absence of school and service, overeating, in an attempt to reduce immediate stress. The immediate reduction of stress acts as a revival, leading to the regularity of symptoms during the premenstrual period.

Socio-Cultural Theory

It hypothesizes that premenstrual dysphoric disorder is a manifestation of the conflict between the social expectations of the dual role of women as productive workers and mothers carrying children. The disorder can be a cultural expression of women’s dissatisfaction with their traditional role in society.

Among the theories above, serotonin has the highest popularity. Although genetic predisposition and social expectations may play a role, the most pioneering scientific data implies serotonin as the primary neurotransmitter whose levels are affected by the level of ovarian steroids. Other neurotransmitter systems that have been implicated are opioid, adrenergic and GABA. – Click here!


Premenstrual dysphoric disorder is a diagnosis used to indicate severe premenstrual stress associated with impairment in the patient’s functioning. The disease is characterized by depressive or labile affection, anxiety, irritability, anger, and other symptoms that occur exclusively during the 2 weeks preceding menstruation. The symptoms may be severe enough to interfere with the individual’s social and professional life, compared to traditional premenstrual syndrome. The disease is a severe medical condition that requires treatment.

The most common symptom is irritability. Common symptoms of chest pain and bloating differ from those of women with major depression. Diagnostic criteria for the disease require the presence of 5 out of 11 symptoms. At least 1 of the first 4 symptoms should occur in the last week of the luteal phase, starting to disappear a few days after the onset of bleeding and absent in the week after menstruation. The symptoms must be severe to interfere with scholastic, social, professional and sexual functioning. The symptoms should be discreetly related to the menstrual cycle and should not aggravate preexisting depression, anxiety or personality disorder. All of the above criteria must be confirmed prospectively daily for at least two menstrual cycles.

Of the 11 symptoms, 10 are emotional and behavioral. Only one has common physical symptoms. Thus, premenstrual dismorphic disorder defines a small group of women with the most severe premenstrual emotional symptoms, with functional impairment.

Research criteria for premenstrual dysphoric disorder include:

  • Marked depressive affectivity, feelings of helplessness, own thoughts of depreciation.
  • Marked anxiety, tension, the feeling of being on the edge of the abyss.
  • Affective lability, marked feelings of sudden sadness or increased rejection sensitivity.
  • Marked and persistent anger and irritability, or increased interpersonal conflicts.
  • Less interest in school, work, friends or small pleasures.
  • The subjective sensation of difficulty in concentration.
  • Lethargy, fatigue, lack of energy.
  • Marked appetite change, overeating.
  • Hypersomnia or insomnia.
  • Subjective sensation of being out of control.
  • Other physical symptoms such as sinus sensitivity or increase in volume, headache, muscle or joint pain, bloating or weight gain.

The disorder greatly interferes with work and school, or with social activities and relationships regarding other people (avoiding social activities, decreasing productivity and efficiency at work and school). The disorder is not an exacerbation of other disorders` symptoms, such as major depression, panic, dysthymic disorder or personality disorder.

Because depression is one of the common symptoms of premenstrual dysphoric disorder, suicide may be possible for these women. A control case study of fertile women with regular menstrual cycles that attempted suicide shows that such attempts during the luteal phase weren`t more common in women with this disorder than those without. This suggests that the disorder is not associated with suicide during the luteal phase, when premenstrual symptoms are present.


Laboratory studies:

  • The role of these studies is limited to the exclusion of differential diagnosis conditions.
  • Thyroid disorders, anemia or perimenopause will be excluded.

Differential diagnosis is made with the following diseases: anemia, anxiety, bipolar affective disorder, chronic fatigue failure syndrome, depression, hyperprolactinemia, hyperthyroidism, hypothyroidism, panic, personality disorders, dysthymic disorder, eating disorders or migraine. – Read more!


The treatment of premenstrual dysphoric disorder includes pharmacological and non-pharmacological therapies. Non-pharmacological activities include aerobic exercise, complex carbohydrate consumption, frequent meals, relaxation, sleep therapy and cognitive-behavioral therapy. The efficacy of lifestyle and psychotherapeutic interventions remains unclear.

Non-Pharmacological Treatment

Relaxation therapy: the relaxation response is a psychological one that causes a decrease in metabolism, heart rate, single-breath, breathing and brain waves. Studies show that therapy is superior to therapy by keeping a daily diary of symptoms or reading a book to relieve physical symptoms.

Light therapy: light emitted by conventional fluorescent lamps is deficient in many of the colors and waves of sunlight. The basis of light therapy is replacing these lamps with full-spectrum fluorescent lamps that are similar to the sun. Their effect is mediated through the serotonin system. – Check this out!

Sleep deprivation: Most patients with major depressive disorder respond to a night of total sleep deprivation. Treatments for major depression can also be effective for this disorder due to their relationship. Studies show that sleep deprivation reduces depression symptoms after a night’s sleep recovery, but not after the night of deprivation.

Cognitive-behavioral therapy: This examines behavioral disorders that are influenced by extreme and negative thoughts. These thoughts are so common that they become automatic and not observed by the patient. Cognitive therapy teaches the patient to examine these thoughts and to replace them with more adaptive ways to look at the events of life. It includes controlling anger, stopping negative thought, reducing negative emotions through cognitive restructuring. While randomized studies show the efficacy of cognitive therapy, the results are not consistent in trials. – Read this!

Pharmacological Treatment

Vitamins and minerals: The use of pyridoxine has been successively variable described in literature. Data on the relief of symptoms of eating disorders after food supplementation are insufficient. Calcium supplementation during the luteal phase has been beneficial to bloating, pain, affection, and appetite.


Drospirenone and ethinyl estradiol are approved for the treatment of disease symptoms in women who choose to use oral contraception. Their efficacy when used for more than 3 menstrual cycles hasn`t been evaluated. Statistically, there`s a significant improvement in symptoms.

Anxiolytics, antidepressants: buspirone has been shown to be effective in the treatment of premenstrual syndrome and premenstrual dysphoric disorder. Side effects include nausea, headache, nervousness, dizziness. It can be given throughout the cycle or during the luteal phase.

Alprazolam has been tested in several clinical trials for its efficacy, but the results are inconsistent; tolerance and addiction are possible effects.

Nonserotoninergic antidepressants, such as maprotilin and bupropion, appear to be ineffective for relieving the symptoms.

Fluoxetine, Sertraline and Paroxetine Were Approved

Fluoxetine was the first serotonin reuptake inhibitor approved to be included in the treatment. Studies show that it`s superior to placebo in reducing symptoms of tension, irritability and dysphoria. Fluoxetine, 20 or 60 mg per day for 6 menstrual cycles, improves affectivity in 52% of cycles, comparable to 28% with placebo. Women who received 60 mg daily reported significantly more adverse effects than those with 20 mg or placebo. Fluoxetine appears to be less effective in controlling the physical symptoms of the disease. The side effects commonly seen are nausea, headache, weight gain, fatigue, insomnia, anxiety, nervousness and drowsiness. A long-term study shows sexual dysfunction and anorgasmia as the most common side effects in 17% of treated patients.

Daily sertraline is more effective than placebo for the treatment of premenstrual dysphoria as a symptomatic relief and alteration of functional impairment. Sertraline administered intermittently only in the luteal phase is more effective than placebo in reducing behavioral and physical symptoms.


Symptoms tend to improve quickly with treatment. After cessation of treatment, symptoms appear rapidly and their recurrence is more predictable than major depression. Symptoms don`t recur after ovariectomy.

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