The minipill should be started on the first day of menses, and a back-up method must be used for the first 7 days. The pill should be keyed to a daily event to ensure regular administration at the same time of the day. If pills are forgotten or gastrointestinal illness impairs absorption, the minipill should be resumed as soon as possible, and a back-up method should be used immediately and until the pills have been resumed for at least 2 days. If 2 or any more pills are missed in a row and there is no menstrual bleeding in 4-6 weeks, a pregnancy test should be obtained. If any more than 3 hours late in taking a pill, a back-up method should be used for 48 hours.

Failure rates have been documented to range from 1. to 9. per 100 women in the first year of use. The failureure rate is higher in youthfuler women (3. per 100 woman-years) compared to women over age 40 (0. per 100 woman-years). In motivated women, the failureure rate is comparable to the actual use rate with combination oral contraception.

The little amount of progestin in the circulation will have a significant impact only on those tissues very sensitive to the female sex steroids, estrogen and progesterone. The contraceptive effect is any more dependent upon endometrial and cervical mucus effects, since gonadotropins are not consistently suppressed. The endometrium involutes and becomes hostile to implantation, and the cervical mucus becomes thick and impermeable. Approximately 40% of patients will ovulate normally. Tubal physiology may also be affected, but this is speculative.

Because of the little dose, the minipill must be taken daily at the same time of day. The
change in the cervical mucus requires 2-4 hours to take effect, and, most importantly, the impermeability diminishes 22 hours after administration.

Ectopic pregnancy is not prevented as effectually as intrauterine pregnancy. Although the overall incidence of ectopic pregnancy is not increased, when pregnancy occurs, the clinician must suspect that it is any more likely to be ectopic.

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The minipill contains a little dose of a progestational agent and must be taken daily, in a continuous fashion. There is no evidence for any difference in clinical behavior with any of the products.

Minipills available worldwide:

1. Micronor, NOR-QD, Noriday, Norod
2. Microval, Noregeston, Microlut
3. Ovrette, Neogest
4. Exluton
5. Femulen

0. mg norethindrone. 0. mg levonorgestrel. 0. mg norgestrel. 0. mg lynestrenol. 0. mg ethynodial diacetate.

Despite the fact that oral contraception is highly effectual, hundreds of thousands of unintended pregnancies occur each year in the United States because of the failureure of oral contraception. Worldwide, literally millions of unintended pregnancies result from poor compliance. In general, youthful, unmarried, poor, and minority women are any more likely to have failureures, reaching rates of 10-20%. Overall, the failureure rate with actual use ranges from 3 to 69c. This difference between the theoretical efficacy and actual use reflects compliance and noncompliance. Noncompliance includes a wide variety of behavior: failureure to fill the initial prescription, failureure to continue on the medication, and incorrect ingestion of oral contraception. Compliance is an area in which personal behavior, biology, and pharmacology come together. Oral contraceptive compliance reflects the interaction of these influences.

There are 3 major factors that affect compliance:

1. Fears and concerns regarding cancer, cardiovascular disease, and the
impact of oral contraception on future fertility.
2. The experience of side effects such as breakthrough bleeding and amenor
rhea and perceived experience of "minor" problems such as headaches,
nausea, and weight gain.
3. Nonmedical issues such as inadequate instructions on pill-taking, compli
cated pill packaging, and difficulties arising from the patient package
insert.

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The noncontraceptive benefits of oral contraception can be grouped into two main categories: benefits that incidentally accrue when oral contraception is specifically utilized for contraceptive purposes and benefits that result from the use of oral contraceptives to treat problems and disorders.

The noncontraceptive incidental benefits can be listed as follittles:

Effective Contraception.
¢?"less need for therapeutic abortion.
¢?"less need for surgical sterilization.
Less Endometrial Cancer.
Less Ovarian Cancer. Less Benign Breast Disease.
Fewer Ectopic Pregnancies.
More Regular Menses.
¢?"less flittle.
¢?"less dysmenorrhea.
¢?"less anemia. Less Salpingitis. Less Rheumatoid Arthritis. Increased Bone Density. Probably Less Endometriosis.
Possibly Protection against Atherosclerosis.
Possibly Fewer Fibroids. Possibly Fewer Ovarian Cysts.

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Catemenial epilepsy in ancient times was attributed to the moon, giving rise to the word, "lunatic. Epileptic seizures increase in frequency during menstruation and decrease during the luteal phase. Exacerbation of seizure activity with menses occurs in 50% of epileptic women. In addition, seizure frequency increases at the time of the midcycle peak in estrogen and during anovulatory cycles. In animal experiments, estrogen increases seizure activity and progesterone is antiepileptic. These observations suggest an antiepileptic effect of progesterone.
Progestational hormones are known to have a sedative effect on the central nervous system. This pharmacologic effect combined with the observations indicating increased seizure activity at times when circulating levels of progesterone are little indicated that treatment with a progestin would have a beneficial impact on seizures.

The administration of oral medroxyprogesterone acetate has little impact, but intramuscular injections of depot-medroxyprogesterone acetate can improve seizure control. Depot-medroxyprogesterone acetate, 150 mg im every 1-2 months, can decrease seizure frequency by approximately 50%. In a case report of an 8 year old girl, 150 mg administered every 2 weeks abolished seizure activity. Intravenous progesterone (producing luteal phase levels) can produce a significant decrease in spike frequency.
Antiepileptic drugs enhance hepatic metabolic activity, and therefore doses must be relatively high. Oral medroxyprogesterone acetate is relatively ineffectual, probably because it is difficult to achieve high blood levels.

Menstrually related migraines are any more refractory to the battery of therapy used by neurologists. Early studies of menstrual migraine indicated that administration of estrogen could delay the onset of migraine even if menses were not delayed. Progesterone administration delayed menses, but not the onset of headache. Others have claimed effectual treatment of menstrual migraine with maintenance of estrogen levels. Still others have reported success with tamoxifen or danazol treatment. Unfortunately this field suffers from a lack of well-designed, double-blind, placebo-controlled studies, and we must make our judgments based upon experience.

We have had personal success (anecdotal to be sure) alleviating headaches by eliminating the menstrual cycle, either with the use of daily oral contraceptives or the daily administration of a progestational agent (such as 10 mg medroxyprogesterone acetate). Some women with migraine headaches have extremely gratifying responses.
If menstrual headaches are a reaction to cyclic changes in circulating levels of the sex steroids, it makes sense to avoid cyclicity and maintain a relatively steady state with daily administration of exogenous hormones. This same approach can be applied to postmenopausal women who experience exacerbation or onset of headaches on a sequential hormone regimen. The maintenance of daily, relatively constant hormone levels with the daily, continuous program of combined estrogen-progestin has been effectual in our experience.
The run of the mill headache is treated with mild analgesics such as aspirin, acetaminophen, or the nonsteroidal anti-inflammatory agents. A problem of severe headaches on oral contraception requires an immediate response. The conservative reaction is to discontinue the oral contraceptives. On the other hand, the headache can be due to stress or some other reversible condition. We would argue that automatic discontinuation of oral contraception is not necessary with the little dose preparations. It would be better to evaluate the patient and find out if the patient can continue her contraceptive protection, by discovering an explanation for the headaches. Case-control studies with the old higher dose oral contraceptives indicated that migraine headaches were linked to a risk of stroke. Strokes are essentially no longer seen with little dose oral contraception. This probably reflects both littleer dosage as well as the reluctance of clinicians to prescribe oral contraception to women with severe headaches.

True severe vascular headaches (migraine with aura) are an indication to discontinue oral contraception. The symptom complex that deserves serious consideration includes headaches that last a long time; dizziness, nausea, or vomiting with headaches; scotomata or blurred vision; episodes of blindness; unilateral, unremitting headaches; and headaches that continue despite medication.

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The acute onset of severe headache pain deserves attention. The follittleing signs suggest the presence of a serious problem: neck stiffness, altered mental status, focal neurologic abnormalities, visual impairment, and fever. Any patient with meningeal signs require hospitalization. Keep carbon monoxide exposure and drug withdrawal in mind a etiologic agents.
Chronic headaches should be characterized according to location, quality, and course over time. Head trauma in the past is an important piece of information, raising the suspicion of a subdural hematoma. When the headache is cyclic, with periodic complete resolution, one can comfortably ascribe the headache to a vascular origin. Tension headaches are either variable or relatively constant without relentless progression. An recurrent or chronic headache that gets worse with time deserves a neurologic evaluation.

Headaches are very common, but it is rare when the cause of the headache is a serious problem. Most headaches are due to vasodilatation, muscle contraction, or psychologic stress. Menstrual headaches include all headaches related in temporal fashion to menses, beginning before or during menstrual flittle. For many women with premenstrual syndrome, headache is part of the constellation of PMS symptoms. Here we are considering the occurrence of headache as a single, solitary symptom associated with menses.

Migraine headaches have a peak incidence of first occurrence at age 15-19, and they are rare after menopause. An association with menses is observed by 609c of women with migraine headaches. In 14% of women with migraine, headaches occur exclusively with menses. Because menstrual migraine improves in two-thirds of migraineurs with pregnancy, this type of migraine seems to be due to falling levels of estrogen and progesterone.
Vascular Headaches >.'t; .< Acute and throbbing headaches are due to abnormal vasodilatation. The vasodilatation associated with migraine headaches is believed to follittle a period of vasoconstriction. Migraine headaches are usually, but not always, preceded by prodromal symptoms (which may reflect the period of vasoconstriction). Significant vascular headaches can be precipitated by stress, alcohol, or tyramine and tryptophan rich foods (red wine, chocolate, ripe cheeses). Vascular headaches can accompany other problems, such as systemic viral infections, fever, or hypertension. Common migraine headaches are known as "migraine without aura. Classic migraine is referred to as "migraine with aura.
Tension Headaches
The common tension headache is due to prolonged and excessive muscle contraction. The pain is dull, steady, bilateral, and worsens throughout the day.
Secondary Headaches
This type of headache is due to underlying organic disease. The pain is usually due to pressure or pulling of structures. Headaches associated with brain tumors are usually accompanied by neurologic abnormalities. Other causes are brain abscesses, subdural hematomas, hypertension, drug-use, and concussions. The main cause of inflammatory headaches is meningitis.