PREMENSTRUAL-SYNDROME - PSYCHIATRIC OR GYNECOLOGICAL DISORDER

The premenstrual syndrome (PMS) is a combination of mental and physical symptoms arising in the luteal phase of the menstrual cycle. The symptoms disappear after the onset of menstruation. During the rest of the follicular phase the patient is free from symptoms. The cyclical nature of the symptom variations is characteristic of the syndrome. The lack of a commonly accepted definition and a way to diagnose PMS has led to contradictory results in the search for its aetiology and treatment. The diagnosis of PMS should be based on prospective daily ratings of symptoms and defined criteria of subgroups. In our studies three subgroups can be identified. The "Pure PMS" group with significant cyclical symptoms being worse during the luteal phase and no symptoms during the follicular phase. A "Premenstrual aggravation" group with symptoms always present but with an aggravation premenstrually. A "Non-PMS" group of women who do not suffer from menstrual cycle related symptoms. These three groups show significant differences in the number of patients with an earlier psychiatric history and are different in the extent of neurosis on a personality test. The Pure PMS group had less neurosis and a lower frequency of patients with an earlier psychiatric history. In anovulatory cycles, whether induced or spontaneous, the cyclical nature of symptoms disappeared. This shows the important role that the corpus luteum has in precipitating symptoms in PMS. GnRH-agonists can be used to induce anovulation and this will stop the cyclical changes. Postmenopausal women receiving oestradiol/progestagen sequential treatment develop PMS-like symptoms when progestagen is added to the treatment. Symptoms seem to be dose dependent related to the oestradiol during the luteal but not the follicular phase. The intracerebral effects that cause the symptoms are still unknown. Progesterone metabolites have, however, been shown to interact with the GABA-A receptor in a similar manner to benzodiazepines and barbiturates, and they also have anxiolytic effects. Progesterone metabolites may occur which have the opposite effect on the GABA-A receptor, producing anxiogenic effects.