Information

14.7: Menstrual Cycle - Biology

14.7: Menstrual Cycle - Biology


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Taboo Topic

The banner in Figure (PageIndex{1}) was carried in a 2014 march in Uganda as part of the celebration of Menstrual Hygiene Day. Menstrual Hygiene Day is an awareness day on May 28 of each year that aims to raise awareness worldwide about menstruation and menstrual hygiene. Maintaining good menstrual hygiene is difficult in developing countries like Uganda because of taboos on discussing menstruation and the lack of availability of menstrual hygiene products. Poor menstrual hygiene, in turn, can lead to embarrassment, degradation, and reproductive health problems in females. May 28 was chosen as Menstrual Hygiene Day because of its symbolism. May is the fifth month of the year that symbolizes the five days of bleeding during menstruation each month. The 28th day was chosen because the menstrual cycle averages about 28 days.

What Is the Menstrual Cycle?

The menstrual cycle refers to natural changes that occur in the female reproductive system each month during the reproductive years. The cycle is necessary for the production of eggs and the preparation of the uterus for pregnancy. It involves changes in both the ovaries and the uterus and is controlled by pituitary and ovarian hormones. Day 1 of the cycle is the first day of the menstrual period, when bleeding from the uterus begins as the built-up endometrium lining the uterus is shed. The endometrium builds up again during the remainder of the cycle, only to be shed again during the beginning of the next cycle if pregnancy does not occur. In the ovaries, the menstrual cycle includes the development of a follicle, ovulation of a secondary oocyte, and the degeneration of the follicle if pregnancy does not occur. Both uterine and ovarian changes during the menstrual cycle are generally divided into three phases, although the phases are not the same in the two organs.

Menarche and Menopause

The female reproductive years are delineated by the start and stop of the menstrual cycle. The first menstrual period usually occurs around 12 or 13 years of age, an event that is known as menarche. There is considerable variation among individuals in the age of menarche. It may occasionally occur as early as eight years of age or as late as 16 years of age and still be considered normal. The average age is generally later in the developing world, and earlier in the developed world. This variation is thought to be largely attributable to nutritional differences.

The cessation of menstrual cycles at the end of a woman’s reproductive years is termed menopause. The average age of menopause is 52 years, but it may occur normally at any age between about 45 and 55 years of age. The age of menopause varies due to a variety of biological and environmental factors. It may occur earlier as a result of certain illnesses or medical treatments.

Variation in the Menstrual Cycle

The length of the menstrual cycle — as well as its phases — may vary considerably, not only among different individuals but also from month to month for a given person. The average length of time between the first day of one menstrual period and the first day of the next menstrual period is 28 days, but it may range from 21 days to 45 days. Cycles are considered regular when a woman’s longest and shortest cycles differ by less than eight days. The menstrual period itself is usually about five days long, but it may vary in length from about two days to seven days.

Ovarian Cycle

The events of the menstrual cycle that take place in the ovaries make up the ovarian cycle. It consists of changes that occur in the follicles of one of the ovaries. The ovarian cycle is divided into the following three phases: the follicular phase, ovulation, and luteal phase. These phases are illustrated in Figure (PageIndex{2}).

Follicular Phase

The follicular phase is the first phase of the ovarian cycle. It generally lasts about 12 to 14 days for a 28-day menstrual cycle. During this phase, several ovarian follicles are stimulated to begin maturing, but usually only one — called the Graafian follicle — matures completely so it is ready to release an egg. The other maturing follicles stop growing and disintegrate. Follicular development occurs because of a rise in the blood level of follicle-stimulating hormone (FSH), which is secreted by the pituitary gland. The maturing follicle releases estrogen, the level of which rises throughout the follicular phase. You can see these and other changes in hormone levels that occur during the menstrual cycle in the chart in Figure (PageIndex{3}).

Ovulation

Ovulation is the second phase of the ovarian cycle. It usually occurs around day 14 of a 28-day menstrual cycle. During this phase, the Graafian follicle ruptures and releases its egg. Ovulation is stimulated by a sudden rise in the blood level of luteinizing hormone (LH) from the pituitary gland. This is called the LH surge. You can see the LH surge in the top hormone graph above. The LH surge generally starts around day 12 of the cycle and lasts for a day or two. The surge in LH is triggered by a continued rise in estrogen from the maturing follicle in the ovary. During the follicular phase, the rising estrogen level actually suppresses LH secretion by the pituitary. However, by the time the follicular phase is nearing its end, the level of estrogen reaches a threshold level above which this effect is reversed, and estrogen stimulates the release of a large amount of LH. The surge in LH matures the egg and weakens the wall of the follicle, causing the fully developed follicle to release its secondary oocyte.

Luteal Phase

The luteal phase is the third and final phase of the ovarian cycle. It typically lasts about 14 days in a 28-day menstrual cycle. At the beginning of the luteal phase, FSH and LH cause the Graafian follicle that ovulated the egg to transform into a structure called a corpus luteum. The corpus luteum secretes progesterone, which in turn suppresses FSH and LH production by the pituitary and stimulates the continued buildup of the endometrium in the uterus. How this phase ends depends on whether or not the egg has been fertilized.

  • If fertilization has not occurred, the falling levels of FSH and LH during the luteal phase cause the corpus luteum to atrophy, so its production of progesterone declines. Without a high level of progesterone to maintain it, the endometrium starts to break down. By the end of the luteal phase, the endometrium can no longer be maintained, and the next menstrual cycle begins with the shedding of the endometrium (menses).
  • If fertilization has occurred so a zygote forms and then divides to become a blastocyst, the outer layer of the blastocyst produces a hormone called human chorionic gonadotropin. This hormone is very similar to LH and preserves the corpus luteum. The corpus luteum can then continue to secrete progesterone to maintain the new pregnancy.

Uterine Cycle

The events of the menstrual cycle that take place in the uterus make up the uterine cycle. This cycle consists of changes that occur mainly in the endometrium, which is the layer of tissue that lines the uterus. The uterine cycle is divided into the following three phases: menstruation, proliferative phase, and secretory phase. These phases are illustrated in Figure (PageIndex{4}).

Menstruation

Menstruation (also called the menstrual period or menses) is the first phase of the uterine cycle. It occurs if fertilization has not taken place during the preceding menstrual cycle. During menstruation, the endometrium of the uterus, which has built up during the preceding cycle, degenerates and is shed from the uterus. The average loss of blood during menstruation is about 35 mL. The flow of blood is often accompanied by uterine cramps, which may be severe in some people.

Proliferative Phase

The proliferative phase is the second phase of the uterine cycle. During this phase, estrogen secreted by cells of the maturing ovarian follicle causes the lining of the uterus to grow, or proliferate. Estrogen also stimulates the cervix of the uterus to secrete larger amounts of thinner mucus that can help sperm swim through the cervix and into the uterus, making fertilization more likely.

Secretory Phase

The secretory phase is the third and final phase of the uterine cycle. During this phase, progesterone produced by the corpus luteum in the ovary stimulates further changes in the endometrium so it is more receptive to implantation of a blastocyst. For example, progesterone increases blood flow to the uterus and promotes uterine secretions. It also decreases the contractility of smooth muscle tissue in the uterine wall.

My body: Menstruators, Not Menstruating Women

Within the field of critical menstruation studies, we must pay attention to our depictions of menstruation and menstruators, and the knowledge we produce in the pursuit to de-stigmatize menstruation. Not all women menstruate, for example, trans women, postmenopausal women, pregnant women, and those experiencing amenorrhea, and not all who menstruate are women, for example, transmen. Experiences of menstruating later in life vary among menstruators as well. Some do not suffer from their periods in direct relation to their gender identity. Others do, as they disidentify with the body as a whole and/or with certain body parts such as the genitalia or the uterus, or with the bodily function of menstruation. This suffering is sometimes related to gender dysphoria. Testosterone treatments are a method adopted by some trans menstruators to get rid of unwanted bleeding. Preventing the menstrual period is not necessarily the main reason for using testosterone, but it can be one among several desired outcomes. Menstruators are of a variety of gender identities (far beyond those who identify as trans) and, hence, menstruation cannot be equated singularly with cis/womanhood.

Review

1. What is the menstrual cycle?

2. Why is the menstrual cycle necessary in order for pregnancy to occur?

3. What organs are involved in the menstrual cycle? What hormones control the cycle?

4. Identify the two major events that mark the beginning and end of the reproductive period in females. When do these events typically occur?

5. Discuss the average length of the menstrual cycle and menstruation, as well as variations that are considered normal.

6. Define the ovarian cycle.

7. Summarize the phases of the ovarian cycle.

8. Compare and contrast events that occur in the ovaries and uterus, depending on whether or not an egg is fertilized during the menstrual cycle.

9. Define the uterine cycle.

10. Give an overview of the phases of the uterine cycle.

11. If the LH surge did not occur in a menstrual cycle, what do you think would happen? Explain your answer.

12. Give one reason why FSH and LH levels drop in the luteal phase of the menstrual cycle.

13. What does the follicle that housed the ovulated egg become in the luteal phase of the menstrual cycle?

14. True or False: Day 1 of the menstrual cycle is when the secondary oocyte is released from its follicle.

15. True or False: The secretory phase of the uterine cycle generally aligns with the luteal phase of the ovarian cycle.

Explore More

Have you ever heard of premenstrual syndrome, also known as PMS? Learn more about what it is and why some women get it here:


Abstract

An analysis of the results of advanced (A) and ordinary (O) level examinations revealed a lower pass-rate, lower distinction-rate, and lower average mark when the examinations were taken during the premenstruum or during menstruation. This was most striking in girls whose menstrual loss continued longer than 6 days and those with menstrual cycles exceeding 31 days. In 42% of the ninety-one girls, whose normal menstrual pattern was known, the stress of the O-level examinations produced an alteration in their menstrual cycle. This resulted in more girls menstruating during examination week than would have been expected from their normal pattern. The tendency was for the cycle to be lengthened rather than shortened, but some girls had temporary amenorrhœa during the examination month.


Contents

The menstrual cycle encompasses the ovarian and uterine cycles. The ovarian cycle describes changes that occur in the follicles of the ovary, [1] whereas the uterine cycle describes changes in the endometrial lining of the uterus. Both cycles can be divided into phases. The ovarian cycle consists of alternating follicular and luteal phases, and the uterine cycle consists of menstruation, the proliferative phase, and the secretory phase. [2] The menstrual cycle is controlled by the hypothalamus and the pituitary gland in the brain. The hypothalamus releases gonadotropin-releasing hormone (GnRH), which causes the nearby anterior pituitary gland to release follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Before puberty, GnRH is released in low steady quantities and at a steady rate. After puberty, GnRH is released in large pulses, and the frequency and magnitude of these determine how much FSH and LH are produced by the pituitary. [3]

Measured from the first day of one menstruation to the first day of the next, the length of a menstrual cycle varies but has a median length of 28 days. [4] The cycle is often less regular at the beginning and end of a woman's reproductive life. [4] At puberty, a child's body begins to mature into an adult body capable of sexual reproduction the first period (called menarche) occurs at around 12 years of age and continues for about 30–45 years. [5] [6] Menstrual cycles end at menopause, which is usually between 45 and 55 years of age. [7] [8]

Ovarian cycle Edit

Between menarche and menopause the human ovaries regularly alternate between luteal and follicular phases during the monthly menstrual cycle. [9] Stimulated by gradually increasing amounts of estrogen in the follicular phase, discharges of blood flow stop and the uterine lining thickens. Follicles in the ovary begin developing under the influence of a complex interplay of hormones, and after several days one, or occasionally two, become dominant, while non-dominant follicles shrink and die. About mid-cycle, some 10–12 hours after the luteinizing hormone (LH) surges, [4] the dominant follicle releases an oocyte, in an event called ovulation. [10]

After ovulation, the oocyte lives for 24 hours or less without fertilization, [11] while the remains of the dominant follicle in the ovary become a corpus luteum – a body with the primary function of producing large amounts of the hormone progesterone. [12] [a] Under the influence of progesterone, the uterine lining changes to prepare for potential implantation of an embryo to establish a pregnancy. The thickness of the endometrium continues to increase in response to mounting levels of estrogen, which is released by the antral follicle (a mature ovarian follicle) into the blood circulation. Peak levels of estrogen are reached at around day thirteen of the cycle and coincide with ovulation. If implantation does not occur within about two weeks, the corpus luteum degenerates into the corpus albicans, which does not produce hormones, causing a sharp drop in levels of both progesterone and estrogen. This drop causes the uterus to lose its lining in menstruation it is around this time that the lowest levels of estrogen are reached. [14]

In an ovulatory menstrual cycle, the ovarian and uterine cycles are concurrent and coordinated and last between 21 and 35 days in an adult woman, with a population average of 27–29 days. [15] Although the average length of the human menstrual cycle is similar to that of the lunar cycle, there is no causal relation between the two. [16]

Follicular phase Edit

The ovaries contain a finite number of egg stem cells, granulosa cells and theca cells, which together form primordial follicles. [12] At around 20 weeks into gestation some 7 million immature eggs have already formed in an ovary. This decreases to around 2 million by the time a girl is born, and 300,000 by the time she has her first period. On average, one egg matures and is released during ovulation each month after menarche. [17] Beginning at puberty, these mature to primary follicles independently of the menstrual cycle. [18] The development of the egg is called oogenesis and only one cell survives the divisions to await fertilization. The other cells are discarded as polar bodies, which cannot be fertilized. [19] The follicular phase is the first part of the ovarian cycle and it ends with the completion of the antral follicles. [9] Meiosis (cell division) remains incomplete in the egg cells until the antral follicle is formed. During this phase usually only one ovarian follicle fully matures and gets ready to release an egg. [20] The follicular phase shortens significantly with age, lasting around 14 days in women aged 18–24 compared with 10 days in women aged 40–44. [14]

Through the influence of a rise in follicle stimulating hormone (FSH) during the first days of the cycle, a few ovarian follicles are stimulated. These follicles, which have been developing for the better part of a year in a process known as folliculogenesis, compete with each other for dominance. All but one of these follicles will stop growing, while one dominant follicle – the one that has the most FSH receptors – will continue to maturity. The remaining follicles die in a process called follicular atresia. [21] Luteinizing hormone (LH) stimulates further development of the ovarian follicle. The follicle that reaches maturity is called an antral follicle, and it contains the ovum (egg cell). [22]

The theca cells develop receptors that bind LH, and in response secrete large amounts of androstenedione. At the same time the granulosa cells surrounding the maturing follicle develop receptors that bind FSH, and in response start secreting androstenedione, which is converted to estrogen by the enzyme aromatase. The estrogen inhibits further production of FSH and LH by the pituitary gland. This negative feedback regulates levels of FSH and LH. The dominant follicle continues to secrete estrogen, and the rising estrogen levels make the pituitary more responsive to GnRH from the hypothalamus. As estrogen increases this becomes a positive feedback signal, which makes the pituitary secrete more FSH and LH. This surge of FSH and LH usually occurs one to two days before ovulation and is responsible for stimulating the rupture of the antral follicle and release of the oocyte. [18] [23]

Ovulation Edit

Around day fourteen, the egg is released from the ovary. [24] Called "ovulation", this occurs when a mature egg is released from the ovarian follicles into the fallopian tube, about 10–12 hours after the peak in LH surge. [4] Typically only one of the 15–20 stimulated follicles reaches full maturity, and just one egg is released. [25] Ovulation only occurs in around 10% of cycles during the first two years following menarche, and by the age of 40–50, the number of ovarian follicles is depleted. [26] LH initiates ovulation at around day 14 and stimulates the formation of the corpus luteum. [2] Following further stimulation by LH, the corpus luteum produces and releases estrogen, progesterone, relaxin (which relaxes the uterus by inhibiting contractions of the myometrium), and inhibin (which inhibits further secretion LH). [22]

The release of LH matures the egg and weakens the follicle wall in the ovary, causing the fully developed follicle to release its oocyte. [27] If it is fertilized by a sperm, the oocyte promptly matures into an ootid, which blocks the other sperm cells and becomes a mature egg. If it is not fertilized by a sperm, the oocyte degenerates. The mature egg has a diameter of about 0.1 mm (0.0039 in), [28] and is the largest human cell. [29]

Which of the two ovaries – left or right – ovulates appears random [30] no left and right coordinating process is known. [31] Occasionally both ovaries release an egg if both eggs are fertilized, the result is fraternal twins. [32] After release from the ovary, the egg is swept into the fallopian tube by the fimbria – a fringe of tissue at the end of each fallopian tube. After about a day, an unfertilized egg disintegrates or dissolves in the fallopian tube, and a fertilized egg reaches the uterus in three to five days. [33]

Fertilization usually takes place in the ampulla, the widest section of the fallopian tubes. A fertilized egg immediately starts the process of embryogenesis (development). The developing embryo takes about three days to reach the uterus, and another three days to implant into the endometrium. It has usually reached the blastocyst stage at the time of implantation: this is when pregnancy begins. [34] The loss of the corpus luteum is prevented by fertilization of the egg. The syncytiotrophoblast (the outer layer of the resulting embryo-containing blastocyst that later becomes the outer layer of the placenta) produces human chorionic gonadotropin (hCG), which is very similar to LH and preserves the corpus luteum. During the first few months of pregnancy, the corpus luteum continues to secrete progesterone and estrogens at slightly higher levels than those at ovulation. After this and for the rest of the pregnancy, the placenta secretes high levels of these hormones – along with human chorionic gonadotropin (hCG), which stimulates the corpus luteum to secrete more progesterone and estrogens, blocking the menstrual cycle. [35] These hormones also prepare the mammary glands for milk [b] production. [35]

Luteal phase Edit

Lasting about 14 days, [4] the luteal phase is the final phase of the ovarian cycle and it corresponds to the secretory phase of the uterine cycle. During the luteal phase, the pituitary hormones FSH and LH cause the remaining parts of the dominant follicle to transform into the corpus luteum, which produces progesterone. [37] [c] The increased progesterone starts to induce the production of estrogen. The hormones produced by the corpus luteum also suppress production of the FSH and LH that the corpus luteum needs to maintain itself. The level of FSH and LH fall quickly, and the corpus luteum atrophies. [39] Falling levels of progesterone trigger menstruation and the beginning of the next cycle. From the time of ovulation until progesterone withdrawal has caused menstruation to begin, the process typically takes about two weeks. For an individual woman, the follicular phase often varies in length from cycle to cycle by contrast, the length of her luteal phase will be fairly consistent from cycle to cycle at 10 to 16 days (average 14 days). [14]

Uterine cycle Edit

The uterine cycle has three phases: menses, proliferative and secretory. [40]

Menstruation Edit

Menstruation (also called menstrual bleeding, menses or a period) is the first and most evident phase of the uterine cycle and first occurs at puberty. Called menarche, the first period occurs at the age of around twelve or thirteen years. [8] The average age is generally later in the developing world and earlier in developed world. [41] In precocious puberty, it can occur as early as age eight years, [42] and this can still be normal. [43] [44]

Menstruation is initiated each month by falling levels of estrogen and progesterone and the release of prostaglandins, [20] which constrict the spiral arteries. This causes them to spasm, contract and break up. [45] The blood supply to the endometrium is cut off and the cells of the top layer of the endometrium (the stratum functionalis) become deprived of oxygen and die. Later the whole layer is lost and only the bottom layer, the stratum basalis, is left in place. [20] An enzyme called plasmin breaks up the blood clots in the menstrual fluid, which eases the flow of blood and broken down lining from the uterus. [46] The flow of blood continues for 2–6 days and around 30–60 milliliters of blood is lost, [15] and is a sign that pregnancy has not occurred. [47]

The flow of blood normally serves as a sign that a woman has not become pregnant, but this cannot be taken as certainty, as several factors can cause bleeding during pregnancy. [48] Menstruation occurs on average once a month from menarche to menopause, which corresponds with a woman's fertile years. The average age of menopause in women is 52 years, and it typically occurs between 45 and 55 years of age. [49] Menopause is preceded by a stage of hormonal changes called perimenopause. [7]

Eumenorrhea denotes normal, regular menstruation that lasts for around the first 5 days of the cycle. [24] Women who experience menorrhagia (heavy menstrual bleeding) are more susceptible to iron deficiency than the average person. [50]

Proliferative phase Edit

The proliferative phase is the second phase of the uterine cycle when estrogen causes the lining of the uterus to grow and proliferate. [39] The latter part of the follicular phase overlaps with the proliferative phase of the uterine cycle. [30] As they mature, the ovarian follicles secrete increasing amounts of estradiol, an estrogen. The estrogens initiate the formation of a new layer of endometrium in the uterus with the spiral arterioles. [2]

As estrogen levels increase, cells in the cervix produce a type of cervical mucus [52] that has a higher pH and is less viscous than usual, rendering it more friendly to sperm. [53] This increases the chances of fertilization, which occurs around day 11 to day 14. [11] This cervical mucus can be detected as a vaginal discharge that is copious and resembles raw egg whites. [54] For women who are practicing fertility awareness, it is a sign that ovulation may be about to take place, [54] but it does not mean ovulation will definitely occur. [15]

Secretory phase Edit

The secretory phase is the final phase of the uterine cycle and it corresponds to the luteal phase of the ovarian cycle. During the secretory phase, the corpus luteum produces progesterone, which plays a vital role in making the endometrium receptive to the implantation of a blastocyst (a fertilized egg, which has begun to grow). [55] Glycogen, lipids, and proteins are secreted into the uterus [56] and the cervical mucus thickens. [57] In early pregnancy progesterone also increases blood flow and reduces the contractility of the smooth muscle in the uterus [22] and raises the woman's basal body temperature. [58]

If pregnancy does not occur the ovarian and uterine cycles start over again. [46]

Only two thirds of overtly normal menstrual cycles are ovulatory, that is, cycles in which ovulation occurs. [15] The other third lack ovulation or have a short luteal phase (less than ten days [59] ) in which progesterone production is insufficient for normal physiology and fertility. [60] Cycles in which ovulation does not occur (anovulation) are common in girls who have just begun menstruating and in women around menopause. During the first two years following menarche, ovulation is absent in around half of cycles. Five years after menarche, ovulation occurs in around 75% of cycles and this reaches 80% in the following years. [61] Anovulatory cycles are often overtly identical to normally ovulatory cycles. [62] Any alteration to balance of hormones can lead to anovulation. Stress, anxiety and eating disorders can cause a fall in GnRH, and a disruption of the menstrual cycle. Chronic anovulation occurs in 6–15% of women during their reproductive years. Around menopause, hormone feedback dysregulation leads to anovulatory cycles. Although anovulation is not considered a disease, it can be a sign of an underlying condition such as polycystic ovary syndrome. [63] Anovulatory cycles or short luteal phases are normal when women are under stress or athletes increasing the intensity of training. These changes are reversible as the stressors decrease or, in the case of the athlete, as she adapts to the training. [59]

Although a normal and natural process, [64] some women experience problems sufficient to disrupt their lives as a result of their menstrual cycle. [65] These include acne, tender breasts, feeling tired, and premenstrual syndrome (PMS). [65] [66] More severe problems such as premenstrual dysphoric disorder are experienced by 3 to 8% of women. [4] [67] Dysmenorrhea or "period pain" [68] can cause cramps in the abdomen, back, or upper thighs that occur during the first few days of menstruation. [69] Debilitating period pain is not normal and can be a sign of something severe such as endometriosis. [70] These issues can significantly affect a woman's health and quality of life and timely interventions can improve the lives of these women. [71]

There are common culturally communicated misbeliefs that the menstrual cycle affects women's moods, causes depression or irritability, or that menstruation is a painful, shameful or unclean experience. Often a woman's normal mood variation is falsely attributed to the menstrual cycle. Much of the research is weak, but there appears to be a very small increase in mood fluctuations during the luteal and menstrual phases, and a corresponding decrease during the rest of the cycle. [72] Changing levels of estrogen and progesterone across the menstrual cycle exert systemic effects on aspects of physiology including the brain, metabolism, and musculoskeletal system. The result can be subtle physiological and observable changes to women's athletic performance including strength, aerobic, and anaerobic performance. [73] Changes to the brain have also been observed throughout the menstrual cycle [74] but do not translate into measurable changes in intellectual achievement – including academic performance, problem-solving, memory, and creativity. [75] Improvements in spatial reasoning ability during the menstruation phase of the cycle are probably caused by decreases in levels of estrogen and progesterone. [72]

In some women, ovulation features a characteristic pain [d] called mittelschmerz (a German term meaning middle pain). The cause of the pain is associated with the ruptured follicle, causing a small amount of blood loss. [20]

Even when normal, the changes in hormone levels during the menstrual cycle can increase the incidence of disorders such as autoimmune diseases, [79] which might be caused by estrogen enhancement of the immune system. [4]

Around 40% of women with epilepsy find that their seizures occur more frequently at certain phases of their menstrual cycle. This catamenial epilepsy may be due to a drop in progesterone if it occurs during the luteal phase or around menstruation, or a surge in estrogen if it occurs at ovulation. Women who have regular periods can take medication just before and during menstruation. Options include progesterone supplements, increasing the dose of their regular anticonvulsant drug, or temporarily adding an anticonvulsant such as clobazam or acetazolamide. If this is ineffective, or when a woman's menstrual cycle is irregular, then treatment is to stop the menstrual cycle occurring. This may be achieved using medroxyprogesterone, triptorelin or goserelin, or by sustained use of oral contraceptives. [80] [81]

Hormonal contraception Edit

Hormonal contraceptives prevent pregnancy by inhibiting the secretion of the hormones, FSH, LH and GnRH. Hormonal contraception that contains estrogen, such as combined oral contraceptive pills (COCs, often referred to as birth control pills) stop the development of the dominant follicle and the mid-cycle LH surge and thus ovulation. [82] Sequential dosing and discontinuation of the COC can mimic the uterine cycle and produce bleeding that resembles a period. In some cases, this bleeding is lighter. [83]

Progestin-only methods of hormonal contraception do not always prevent ovulation but instead work by stopping the cervical mucus from becoming sperm-friendly. Hormonal contraception is available in a variety of forms such as pills, patches, skin implants and hormonal intrauterine devices (IUDs). [84]

Most female mammals have an estrous cycle, but only ten primate species, four bat species, the elephant shrews and the spiny mouse have a menstrual cycle. [85] The cycles are the same as in humans apart from the length, which ranges from 21 to 37 days. [86] The lack of immediate relationship between these groups suggests that four distinct evolutionary events have caused menstruation to arise. [87] In species that have a menstrual cycle, ovulation is not obvious to potential mates and there is no mating season. [88] [89] There are four theories on the evolutionary significance of menstruation: [87]


This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original authors and the source are credited.

Brandes JL: Migraine in women. Continuum (Minneap Minn) 2012, 18: 835–852.

Peng KP, Wang SJ: Migraine diagnosis: screening items, instruments, and scales. Acta Anaesthesiol Taiwan 2012, 50: 69–73. 10.1016/j.aat.2012.05.002

Ward TN: Migraine diagnosis and pathophysiology. Continuum (Minneap Minn) 2012, 18: 753–763.

Rizzoli PB: Acute and preventive treatment of migraine. Continuum (Minneap Minn) 2012, 18: 764–782.

Allais G, Castagnoli Gabellari I, De Lorenzo C, et al.: Menstrual migraine: clinical and therapeutical aspects. Expert Rev Neurother 2007, 7: 1105–1120. 10.1586/14737175.7.9.1105

Martin VT, Lipton RB: Epidemiology and biology of menstrual migraine. Headache 2008,48(Suppl 3):S124–130.

Brandes JL, Poole A, Kallela M, et al.: Short-term frovatriptan for the prevention of difficult-to-treat menstrual migraine attacks. Cephalalgia 2009, 29: 1133–1148. 10.1111/j.1468-2982.2009.01840.x

Headache Classification Subcommittee of the International Headache Society: The international classification of headache disorders: 2nd edition. Cephalalgia 2004,24(Suppl 1):9–160.

Calhoun AH: Current topics and controversies in menstrual migraine. Headache 2012,52(Suppl 1):8–11.

Bussone G, Allais G, Castagnoli Gabellari I, et al.: Almotriptan for menstrually related migraine. Expert Opin Pharmacother 2011, 12: 1933–1943. 10.1517/14656566.2011.594794

Russell MB: Genetics of menstrual migraine: the epidemiological evidence. Curr Pain Headache Rep 2010, 14: 385–388. 10.1007/s11916-010-0142-6

Colson N, Fernandez F, Griffiths L: Genetics of menstrual migraine: the molecular evidence. Curr Pain Headache Rep 2010, 14: 389–395. 10.1007/s11916-010-0129-3

Von Seggern RL, Mannix LK, Adelman JU: Rofecoxib in the prevention of perimenstrual migraine: an open-label pilot trial. Headache 2004, 44: 160–165. 10.1111/j.1526-4610.2004.04033.x

MacGregor EA, Frith A, Ellis J, et al.: Prevention of menstrual attacks of migraine: a double-blind placebo-controlled crossover study. Neurology 2006, 67: 2159–2163. 10.1212/01.wnl.0000249114.52802.55

Almen-Christensson A, Hammar M, Lindh-Astrand L, et al.: Prevention of menstrual migraine with perimenstrual transdermal 17-beta-estradiol: a randomized, placebo-controlled, double-blind crossover study. Fertil Steril 2011,96(498–500):e491.

Allais G, Sanchez del Rio M, Diener HC, et al.: Perimenstrual migraines and their response to preventive therapy with topiramate. Cephalalgia 2011, 31: 152–160. 10.1177/0333102410378049

Nelles G, Schmitt L, Humbert T, et al.: Prevention of episodic migraines with topiramate: results from a non-interventional study in a general practice setting. J Headache Pain 2010, 11: 33–44. 10.1007/s10194-009-0163-x

Facchinetti F, Sances G, Borella P, et al.: Magnesium prophylaxis of menstrual migraine: effects on intracellular magnesium. Headache 1991, 31: 298–301. 10.1111/j.1526-4610.1991.hed3105298.x

Giacovazzo M, Gallo MF, Guidi V, et al.: Nimesulide in the treatment of menstrual migraine. Drugs 1993,46(Suppl 1):140–141.

Guidotti M, Mauri M, Barrila C, et al.: Frovatriptan vs. transdermal oestrogens or naproxen sodium for the prophylaxis of menstrual migraine. J Headache Pain 2007, 8: 283–288. 10.1007/s10194-007-0417-4

Casolla B, Lionetto L, Candela S, et al.: Treatment of perimenstrual migraine with triptans: an update. Curr Pain Headache Rep 2012, 16: 445–451. 10.1007/s11916-012-0280-0

Tfelt-Hansen PC: Published and not fully published double-blind, randomised, controlled trials with oral naratriptan in the treatment of migraine: a review based on the GSK Trial Register. J Headache Pain 2011, 12: 399–403. 10.1007/s10194-011-0327-3

Sanford M: Frovatriptan: a review of its use in the acute treatment of migraine. CNS Drugs 2012, 26: 791–811. 10.2165/11209380-000000000-00000

Bartolini M, Giamberardino MA, Lisotto C, et al.: Frovatriptan versus almotriptan for acute treatment of menstrual migraine: analysis of a double-blind, randomized, cross-over, multicenter, Italian, comparative study. J Headache Pain 2012, 13: 401–406. 10.1007/s10194-012-0455-4

Allais G, Castagnoli Gabellari I, Mana O, et al.: Treatment strategies for menstrually related migraine. Womens Health (Lond Engl) 2012, 8: 529–541. 10.2217/whe.12.37

Headache Classification Committee of the International Headache Society: Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Headache classification committee of the international headache society. Cephalalgia 1988,8(Suppl 7):1–96.

Tuchman M, Hee A, Emeribe U, et al.: Efficacy and tolerability of zolmitriptan oral tablet in the acute treatment of menstrual migraine. CNS Drugs 2006, 20: 1019–1026. 10.2165/00023210-200620120-00005

Facchinetti F, Allais G, Nappi RE, et al.: Sumatriptan (50 mg tablets vs. 25 mg suppositories) in the acute treatment of menstrually related migraine and oral contraceptive-induced menstrual migraine: a pilot study. Gynecol Endocrinol 2010, 26: 773–779. 10.3109/09513590.2010.487607

Savi L, Omboni S, Lisotto C, et al.: Efficacy of frovatriptan in the acute treatment of menstrually related migraine: analysis of a double-blind, randomized, cross-over, multicenter, Italian, comparative study versus rizatriptan. J Headache Pain 2011, 12: 609–615. 10.1007/s10194-011-0366-9

Brandes JL, Smith T, Diamond M, et al.: Open-label, long-term tolerability of naratriptan for short-term prevention of menstrually related migraine. Headache 2007, 47: 886–894. 10.1111/j.1526-4610.2007.00809.x

Jadad AR, Moore RA, Carroll D, et al.: Assessing the quality of reports of randomized clinical trials: is blinding necessary? Control Clin Trials 1996, 17: 1–12. 10.1016/0197-2456(95)00134-4

Brigo F, Storti M, Nardone R, et al.: Transcranial magnetic stimulation of visual cortex in migraine patients: a systematic review with meta-analysis. J Headache Pain 2012, 13: 339–349. 10.1007/s10194-012-0445-6

Silberstein SD, Elkind AH, Schreiber C, et al.: A randomized trial of frovatriptan for the intermittent prevention of menstrual migraine. Neurology 2004, 63: 261–269. 10.1212/01.WNL.0000134620.30129.D6

Newman L, Mannix LK, Landy S, et al.: Naratriptan as short-term prophylaxis of menstrually associated migraine: a randomized, double-blind, placebo-controlled study. Headache 2001, 41: 248–256. 10.1046/j.1526-4610.2001.111006248.x

Mannix LK, Savani N, Landy S, et al.: Efficacy and tolerability of naratriptan for short-term prevention of menstrually related migraine: data from two randomized, double-blind, placebo-controlled studies. Headache 2007, 47: 1037–1049. 10.1111/j.1526-4610.2007.00855.x

Tuchman MM, Hee A, Emeribe U, et al.: Oral zolmitriptan in the short-term prevention of menstrual migraine: a randomized, placebo-controlled study. CNS Drugs 2008, 22: 877–886. 10.2165/00023210-200822100-00007

Silberstein SD, Berner T, Tobin J, et al.: Scheduled short-term prevention with frovatriptan for migraine occurring exclusively in association with menstruation. Headache 2009, 49: 1283–1297. 10.1111/j.1526-4610.2009.01509.x

Lionetto L, Casolla B, Mastropietri F, et al.: Pharmacokinetic evaluation of zolmitriptan for the treatment of migraines. Expert Opin Drug Metab Toxicol 2012, 8: 1043–1050. 10.1517/17425255.2012.701618

Loder E: Prophylaxis of menstrual migraine with triptans: problems and possibilities. Neurology 2002, 59: 1677–1681. 10.1212/01.WNL.0000034179.17926.2D


Materials and Methods

Data obtained from 50 women enrolled in our initial study, which documented two and three follicular waves [ 64], were carefully evaluated to elucidate different patterns of follicle-wave development. Participants were assessed, by history and physical examination, to be healthy women of reproductive age (mean ± SD = 28.0 ± 6.9 yr, range = 19–43 yr). Women who were currently or recently pregnant or lactating, had used hormonal contraception within 3 mo of enrollment, had a history of irregular menstrual cycles, or were taking medication(s) known or suspected to interfere with reproductive function were not eligible to participate. Informed consent was obtained from all women prior to initiating study procedures. The study protocol was approved by the Institutional Review Board of the University of Saskatchewan.

Each volunteer underwent daily transvaginal ultrasonographic evaluation of her ovaries for one interovulatory interval (IOI). An IOI was defined as the interval from one ovulation to the subsequent ovulation. Ultrasound examinations were initiated 12 days after menses (i.e., a few days before the first ovulation) and were continued until 3 days after the second ovulation. Ovulation was defined as the disappearance of a large follicle (>15 mm) that had been identified by ultrasonography on the previous day, and the subsequent visualization of a corpus luteum [ 41, 82]. Follicles ≥2 mm were measured during each examination, and the number of follicles ≥5 mm tabulated. The length and width of each follicle were measured in both the sagittal and transverse planes. Follicle diameter was then calculated by averaging the mean measurement in the sagittal plane by the mean measurement in the transverse plane. The methods used for tracking follicle diameter and follicle number each day during the IOI are as described in Baerwald et al. [ 64].

High-resolution Ultramark 9 and ATL HDI 5000 ultrasound machines with 5–9 MHz multifrequency convex array transducers (Advanced Technologies Laboratories, Bothell, WA) were used to acquire follicular data. Approximately 90% of the examinations were performed by one sonographer (ARB). A second sonographer (RAP) was available when the primary sonographer was not available.

Follicular waves were characterized by an increase and subsequent decrease in the number of follicles ≥5 mm, occurring in association with the growth of at least two follicles to ≥6 mm, as documented in the previous report [ 64]. In the present analysis, major waves were defined as waves in which one follicle grew to ≥10 mm and exceeded the next largest follicle by ≥2 mm (i.e., development of a dominant follicle). Minor waves were defined as those in which the largest follicle developed to <10 mm and did not grow larger than all other follicles of the wave by ≥2 mm (i.e., no evidence of follicular dominance). Wave emergence was defined as the day at which the largest follicle of each wave was first identified, retrospectively, at 4–5 mm. An interwave interval (IWI) was defined as the interval from the emergence of one wave to the emergence of the subsequent wave. Selection was defined as the day on which the prospective dominant follicle became, and remained, larger than all other follicles of a major wave.

Blood samples were drawn every third day during the IOI in a stratified manner among women so that each day of the IOI was represented. The stratification scheme was used to randomly assign one third of the women to have blood drawn on Days 1, 4, 7, etc., one third on Days 2, 5, 8, etc., and the remaining one third on days 3, 6, 9, etc. Blood was collected into a 7-ml clot-activated tube and allowed to sit at room temperature for 15–30 min before centrifugation for 10 min at 3000 rpm (700 × g). The serum was drawn off and stored at −20°C. Sequential competitive fluorescence immunoassays (Immulite Diagnostic Products Corporation, Los Angeles, CA) were performed to measure serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estradiol-17β (E2). Interassay coefficients of variation were as follows: LH (low = 6.3%, medium = 4.0%, high = 4.5%), FSH (low = 8.0%, medium = 2.9%, high = 4.1%), and E2 (low = 9.8%, medium = 5.6%, high = 4.3%). Minimal detectable limits were 0.1 mIU/ml for FSH, 0.1 mIU/mL for LH, and 15 pg/ml for E2.

We initially categorized follicle diameter, follicle number, and endocrine data into two- or three-wave patterns [ 64]. In the present study, data were further partitioned into major and minor wave patterns: minor major (− +), major major (+ +), minor minor major (− − +), minor major major (− + +), and major major major (+ + +). Follicle and endocrine data were centralized to the day of wave emergence and normalized to the mean IOI of the respective wave patterns.

In women with two follicular waves, t-tests were used to compare − + and + + wave cycles with respect to days of wave emergence, IOI, IWI, maximum number of follicles ≥5 mm, follicle diameter, growth rate, and regression rate (SPSS Version 11, 2002). In women with three follicular waves, analyses of variance with the Scheffe post hoc tests were used to compare endpoints between − − +, − + +, and + + + wave cycles (SPSS Version 11, 2002). Student t-tests and repeated measures analyses (SPSS Version 11, 2002 PROC MIXED, SAS/STAT Software, 2002) were used to compare IWI, follicle diameter, growth rate, and regression rate between waves. Repeated measures analyses (PROC MIXED, SAS/STAT Software, 2002) were also used to assess changes in follicle diameter, follicle number, and endocrine status during the IOI.


Menopause and FSH Levels

FSH or follicle stimulating hormone is a crucial hormone for regulating the reproductive processes of the body. In women older than 45 years, high FSH levels may indicate an impending menopause. Know more about the relation between FSH levels and menopause in this article.

FSH or follicle stimulating hormone is a crucial hormone for regulating the reproductive processes of the body. In women older than 45 years, high FSH levels may indicate an impending menopause. Know more about the relation between FSH levels and menopause in this article.

Menopause can be a difficult phase in the life of many women, as they have to deal with some uncomfortable menopausal symptoms, like irregularities in the menstrual cycle, irritability, depression, sleep disorders, and hot flashes, to name a few.

Menopause is actually a process, or a transition period from having regular menstrual cycle to its complete cessation, and during this period, women can experience a lot of irregularities in their menstrual cycle. A major part of the frustration, however, comes from the uncertainty of the fact that whether these are the symptoms of impending menopause, or an indicator of some other health problems.

Would you like to write for us? Well, we're looking for good writers who want to spread the word. Get in touch with us and we'll talk.

But nowadays, there are certain tests, such as FSH test that can help a woman know, if irregularities in her menstrual cycle is caused by approaching menopause or by some other factors. So, let’s find out what is FSH and its association with menopause.

FSH stands for follicle-stimulating hormone, a hormone secreted by the pituitary gland. This hormone is responsible for regulating growth and development, as well as pubertal maturation in both male and female. It plays a key role in the reproductive processes of the human body.

In women, FSH stimulates the growth of the ovarian follicles and estrogen production, by the ovaries. The hormone also regulates ovulation. A high level of FSH induces ovulation, i.e. the release of an egg by the ovary. When an egg is released by the ovary, the level of FSH decreases in the body, while that of estrogen rises.

The main function of FSH in a menstruating women, is to stimulate the ovarian follicles that contain the eggs. This stimulation causes one of the ovarian follicle to grow and release an egg, after which the level of FSH decreases in the body. In case of menopause, there will not be any drop in the level of FSH, due to the absence of ovulation. Menopause, which marks the end of the menstrual cycle is therefore, characterized by high FSH levels.

Menopause is also characterized by a marked reduction in the level of the hormone, estrogen. As a result, the body signals the pituitary gland to produce more FSH, so that it can promote the ovaries to increase the production of estrogen. But, even a high level of FSH during menopause fails to stimulate the growth of the ovarian follicles, induce ovulation, and increase the level of estrogen.

However, the pituitary gland still tries its best to induce ovulation by continuing to increase the level of FSH. This is the reason why the level of FSH in the body remains high after menopause. In other words, a consistently high level of FSH may indicate that the ovaries are failing and the woman is approaching menopause. The medical definition of menopause is absence of menstrual cycles for 12 consecutive months.

Would you like to write for us? Well, we're looking for good writers who want to spread the word. Get in touch with us and we'll talk.

The FSH level can be determined with the help of blood, urine, or saliva test. The over-the-counter test kits usually check urine or saliva for the level of FSH. The urine tests are usually 90% accurate, while the saliva tests are not so accurate, as their results can be influenced by several factors, including the use of oral contraceptives and smoking. FSH test is mainly used to find out whether a woman is experiencing irregular menstruation as a premenopausal symptom, or it is caused by certain other factors. A high FSH level can indicate that the body is trying to induce ovulation, but is failing to do so.

FSH test also helps distinguish between primary ovarian failure and secondary ovarian failure. Primary ovarian failure is caused by the failure of the ovaries themselves, while secondary ovarian failure may be associated with some underlying disorders of the hypothalamus and pituitary gland. Conditions other than menopause, that have been found to cause a high level of FSH are, infertility, and polycystic ovarian syndrome. FSH test is also used to evaluate the condition of early sexual development in children and infertility in men.

Women who are not menstruating, can take the FSH test at any time. But, women in the reproductive stage, should keep in mind that, the level of FSH can fluctuate during the menstrual cycle, and hence, the test should be carried out on a specific day, usually on the third day of the menstrual cycle. Follow-up tests are required to be done, usually after a month.

While evaluating the FSH test results, it should always be kept in mind that the level of this hormone vary depending on your age. For menstruating women, the normal values for FSH blood test, is 4.7 mlU/ml to 21.5 mlU/ml, while for post-menopausal women, it is 25.8 mIU/ml to 134.8 mIU/ml. If the level is higher than 25, then the woman may be in the peri or premenopausal stage, while she is approaching menopause, if the level is around 50.

However, the normal range for FSH can vary from lab to lab, which should be considered while evaluating the results of the test. Further, factors like, taking birth control pills, and hormone replacement therapy, can affect the results of the test.

Before coming to any conclusion regarding the results of FSH test, it should be kept in mind that not all medical communities consider it as a reliable test for determining whether a woman is going through perimenopause or menopause. Women in their 40s and 50s can experience a lot of fluctuations in their menstrual cycle. They may skip a few periods, then have periods for a few months and then again skip them.

The results of FSH tests done when the periods are irregular, can vary greatly. If the test is done while you are having menstrual cycle, it may show normal values, even if you are going through perimenopause and experiencing the menopausal symptoms. Depending on factors like stress, diet, and overall health, a woman can move in and out of perimenopause, and hence, a single value of FSH is not adequate to declare whether you are in menopause. Moreover, conditions other than menopause can also cause the level of FSH to rise in the body, as mentioned already.

So, if the result of FSH test is positive, i.e., if your FSH levels are high, then it is better to talk to your physician, instead of drawing any conclusion. The same goes for those women who have normal FSH level, but are experiencing the troublesome symptoms of menopause. Menopause can be confirmed only by the absence of menstrual cycles for 12 consecutive months. A single hormone test cannot confirm menopause, though the results of lab tests done over a period of time, along with a detailed study of the medical history of the woman and her symptoms, can help assess the condition.

Disclaimer: This article is for informative purposes only, and should not be treated as a substitute for professional medical advice.


Menstrual hygiene products

Several menstrual hygiene products exist for menstrual management. 𖏫] Such products are used especially in order to avoid damage to clothing. They are commonly used in the West, but are less available in some underdeveloped parts of the world. Such products include sanitary napkins and tampons (which are disposable) cloth menstrual pad and menstrual cups (which are reusable). Various improvised products may also be used, especially in the developing world, such as cotton, cloth, toilet paper. In recent years, the problem of inaccessibility to these products has come to light and has become a center of debate in regards to abolishing the excess tax on them or making them completely free. In 2018, Scotland became the first country in the world to “provide free menstrual pads in schools and colleges in an effort to ban period poverty” and the UK followed a similar path in 2019, announcing a campaign to “end period poverty globally by 2030.“ 𖏬]

Seclusion during menstruation

In some cultures, females are isolated during menstruation, as they are seen as unclean, dangerous, or bringing bad luck to those who encounter them. These practices are common in parts of South Asia, especially in Nepal. Chhaupadi is a social practice that occurs in the western part of Nepal for Hindu women, which prohibits a woman from participating in everyday activities during menstruation. Women are considered impure during this time, and are kept out of the house and have to live in a shed. Although chhaupadi was outlawed by the Supreme Court of Nepal in 2005, the tradition is slow to change. 𖏭] 𖏮] Women and girls in cultures which practice such seclusion are often confined to menstruation huts, which are places of isolation used by cultures with strong menstrual taboos. The practice has recently come under fire due to related fatalities. Nepal criminalized the practice in 2017 after deaths were reported after the elongated isolation periods, but “the practice of isolating menstruating women and girls continues.“ 𖏯]

Etymological

The word "menstruation" is etymologically related to "moon". The terms "menstruation" and "menses" are derived from the Latin mensis (month), which in turn relates to the Greek mene (moon) and to the roots of the English words month and moon. 𖏰]

The Moon

Even though the average length of the human menstrual cycle is similar to that of the lunar cycle, in modern humans there is no relation between the two. 𖏱] The relationship is believed to be a coincidence. 𖏲] 𖏳] Light exposure does not appear to affect the menstrual cycle in humans. ⎗] A meta-analysis of studies from 1996 showed no correlation between the human menstrual cycle and the lunar cycle, 𖏴] nor did data analysed by period-tracking app Clue, submitted by 1.5m women, of 7.5m menstrual cycles, however the lunar cycle and the average menstrual cycle were found to be basically equal in length. 𖏵]

Dogon villagers did not have electric lighting and spent most nights outdoors, talking and sleeping, so they were apparently an ideal population for detecting a lunar influence none was found. 𖏶]

In a number of countries, mainly in Asia, legislation or corporate practice has introduced formal menstrual leave to provide women with either paid or unpaid leave of absence from their employment while they are menstruating. 𖏷] Countries with policies include Japan, Taiwan, Indonesia, and South Korea. 𖏷] The practice is controversial in western cultures due to concerns that it bolsters the perception of women as weak, inefficient workers, 𖏷] as well as concerns that it is unfair to men. 𖏸] 𖏹]


Conclusion

Here we identified 140 unique differentially expressed miRNAs between AD patients and healthy controls. Using a signature of 12 miRNAs differentially expressed between AD patients and healthy controls we were not only able to distinguish with high diagnostic accuracies between AD patients and healthy controls, but also between AD patients and patients suffering from other neurological disorders including mild cognitive impairment as a potential preliminary stage of AD, and other neurodegenerative diseases like PD and multiple sclerosis as well as mental diseases like SCHIZ, DEP, and BD. However, additional work will be needed to elucidate the applicability of this 12-miRNA signature as a potential diagnostic test for AD and the above-mentioned effects of the drug treatments commonly used in the treatment of the disease. Hopefully, tests of this non-invasive and relatively cheap kind will be applicable to prodromal AD cases and to MCI patients with the aim to recognize early AD to initiate treatment.


Methods

This study adhered to the research guidelines and ethical protocols of Wageningen University in the Netherlands. Thirty respondents, ten of whom were male were interviewed from September 1996 to September 2000 [19]. The respondents were obtained by snowball sampling, and were found in thirteen different sites, 12 in Trinidad (Paramin, Talparo, Sangre Grande, Mayaro, Carapichaima, Kernahan, Newlands, Todd's Road, Arima, Guayaguayare, Santa Cruz, Port of Spain and Siparia) and one in Tobago (Mason Hall). Snowball sampling was used because there was no other means of identifying respondents. The chief objective of the sampling method was to identify knowledgeable respondents no priority was given to extrapolating the data to the wider population to establish prevalence of use. No statistical analysis is applied to the data since this would have required the use of a random sample thus increasing the risk of not identifying knowledgeable respondents.

Twenty respondents were interviewed once, the other ten (who were healers) were interviewed three or four times. Healers were also asked to reconstruct the circumstances and contexts of the plant uses so that the means of administration of the plants could be identified. No interview schedule of questions was used but a more qualitative, conversational technique. Plants were collected when available to verify that the common names used by each respondent were the same in each ethnic group as those recorded in the literature. The majority of the plants were identified at the Herbarium of the University of the West Indies but voucher samples were not deposited. This ethnomedicinal study was part of a larger research project on ethnoveterinary medicine [11, 18].

Validation of practices

A preliminary validation of ethnomedicinal practices ensures that clinical trials are not wasted on plants that are used solely for cultural or religious reasons. The validation of the remedies was conducted with a non-experimental method [11, 18, 19]. This method consists of:

1. obtaining an accurate botanical identification,

2. determining whether the folk data can be understood in terms of bioscientific concepts and methods,

3. searching the chemical/pharmaceutical/pharmacological literature for the plant's known chemical constituents and to determine the known physiological effects of either the crude plant, related species, or isolated chemical compounds that the plant is known to contain. This information is used to assess whether the plant use is based on empirically verifiable principles or whether symbolic aspects of healing are of greater relevance. If ethnobotanical data, phytochemical and pharmacological information supports the folk use of a plant species it can be grouped into the validation level with the highest degree of confidence.

Four levels of validity were established [19]:

1. If no information supports the use it indicates that the plant may be inactive or no research has been done on the plant.

2. A plant (or closely related species of the same genus), which is used in geographically or temporally distinct areas in the treatment of similar illnesses, attains the lowest level of validity, if no further phytochemical or pharmacological information validates the popular use. Use in other areas increases the likelihood that the plant is active against the illness.

3. If in addition to the ethnobotanical data, phytochemical or pharmacological information also validates the use in Trinidad, the plant may exert a physiological action on the patient and is more likely to be effective than those at the lowest level of validity.

4. If ethnobotanical [20], phytochemical and pharmacological data supports the folk use of the plant, it is grouped in the highest level of validity and is most likely an effective remedy.

A comparable validation process was used to examine the plants used by traditional healers of ancient Persia to induce abortions [21]. The authors evaluated the validity and the efficacy of the plants used by (1) comparing other reported uses of these plants in traditional medicine, (2) investigating the medical and pharmacological literature on the medicinal properties of the plant species used, and (3) investigating the reported cytotoxic effects of compounds prevalent in these plants.


Dysmenorrhoea

Dickerson E, Raghunath AS, Atkin SL. Rational testing: initial investigation of amenorrhoea. BMJ. 2009339:b2184.

Wellman M. Investigating primary and secondary amenorrhoea. Medicine Today. 201516(11):27-32.

Teede H, Misso M, Costello M, Dokras A, Laven J, Moran L. International evidence-based guideline for the assessment and management of polycystic ovary syndrome 2018. Melbourne, Victoria: Monash University 2018. Available from: https://www.monash.edu/__data/assets/pdf_file/0004/1412644/PCOS_Evidence-Based-Guidelines_20181009.pdf.

Practice Committee of the American Society for Reproductive Medicine. Current evaluation of amenorrhea. Fertil Steril. 200890(suppl 5):S219-25.

Pitts M, Ferris JA, Smith AMA, Shelley JM, Richters J. Prevalence and correlates of three types of pelvic pain in a nationally representative sample of Australian women. MJA. 2008189(3):138-43.

Reddish S. Dysmenorrhoea. Aust Fam Physician. 200635(11):846-9.

National Institute for Health and Care Excellence (NICE). Endometriosis: diagnosis and management. NG73. NICE 2017. Available from: https://www.nice.org.uk/guidance/ng73.

European Society of Human Reproduction and Embryology. ESHRE guideline for the diagnosis and treatment of endometriosis. ESHRE 2007 [updated 2007 June 30]. Available from: http://guidelines.endometriosis.org/introduction.html.

European society of Human Reproduction and Embryology (ESHRE) Endometriosis Guideline Development Group. Management of women with endometriosis. ESHRE 2013. Available from: https://www.eshre.eu/Guidelines-and-Legal/Guidelines/Endometriosis-guideline.aspx.

Petraglia F, Hornung D, Seitz C, Faustmann T, Gerlinger C, Luisi S, et al. Reduced pelvic pain in women with endometriosis: efficacy of long-term dienogest treatment. Arch Gynecol Obstet. 2012285(1):167-73.

Vannuccini S, Luisi S, Tosti C, Sorbi F, Petraglia F. Role of medical therapy in the management of adenomyosis. Fertility and Sterility. 2018109(3):398-405.

Osada H. Uterine adenomyosis and adenomyoma: the surgical approach. Fertility and Sterility. 2018109(3):406-17.

National Institute for Health and Care Excellence (NICE). Heavy Menstrual Bleeding: Assessment and Management. NG88. NICE 2018 [updated 2018 Mar]. Available from: https://www.nice.org.uk/guidance/ng88.

Munro M, Critchley HO, Fraser IS, FIGO Menstrual Disorders Working Group. The FIGO classification of causes of abnormal uterine bleeding in the reproductive years. Fertil Steril. 201195(7):2204-8.

Munro M, Critchley HO, Broder MS, Fraser IS, FIGO Working Group of Menstrual Disorders. FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. Int J Gynaecol Obstet. 2011113(1):3-13.

Australian Commission on Safety and Quality in Healthcare (ACSQHC). Heavy Menstrual Bleeding Clinical Care Standard. Sydney: ACSQHC 2017. Available from: https://www.safetyandquality.gov.au/standards/clinical-care-standards/heavy-menstrual-bleeding-clinical-care-standard.

National Institute for Health and Care Excellence (NICE). Heavy Menstrual Bleeding: Assessment and Management. NG88. NICE 2007 [updated: 2016 Aug].

Bateson D, Black K. Heavy menstrual bleeding: Treatment and referral options. Medicine Today. 201819(5):27-32.

Dickerson K, Menon N, Zia A. Abnormal uterine bleeding in young women with blood disorders. Pediatr Clin North Am. 201865(3):543-60.

Department of Health. Understanding the National Cervical Screening Program Management Pathway: A Guide for Healthcare Providers. Australian Government 2017 [updated 2019 Nov 27]. Available from: https://www.health.gov.au/resources/publications/national-cervical-screening-program-understanding-the-national-cervical-screening-program-management-pathway.

Jensen J, Parke S, Mellinger U, Machlitt A, Fraser IS. Effective treatment of heavy menstrual bleeding with estradiol valerate and dienogest: a randomized controlled trial. Obstet Gynecol. 2011117(4):777-87.

The Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG). College statement C-Gyn 23: Uterine artery embolisation for the treatment of uterine fibroids. [Internet]. RANZCOG 2008 [updated 2014]. Available from: https://ranzcog.edu.au/RANZCOG_SITE/media/RANZCOG-MEDIA/Women%27s%20Health/Statement%20and%20guidelines/Clinical%20-%20Gynaecology/Uterine-Artery-Embolisation-(C-Gyn-23)_2.pdf?ext=.pdf.

Abnormal Vaginal Bleeding in Pre- and Peri-Menopausal Women: A Diagnostic Guide for General Practitioners Gynaecologists [internet]. The Royal Australian and New Zealand College of Radiologists, Cancer Australia, National Centre for Gynaecological Cancers: Australian Government 2011. Available from: https://www.canceraustralia.gov.au/publications-and-resources/cancer-australia-publications/abnormal-vaginal-bleeding-pre-peri-and-post-menopausal-women-diagnostic-guide-general-practitioners.

McPherson K, Metcalfe MA, Herbert A, Maresh M, Casbard A, Hargreaves J, et al. Sever complications of hysterectomy: the VALUE study. BJOG: an International Journal of Obstetrics and Gynaecology. 2004111:688-94.

Ely J, Kennedy CM, Clark EC, Bowdler NC. Abnormal Uterine Bleeding: A Management Algorithm. J Am Board Fam Med. 200619(6):590-602.

Read C, May T, Stellingwerff M. How to Treat: Irregular Vaginal Bleeding Australian Doctor 200718(May):27 -34.

Selo-Ojeme D, Dayoubi N, Patel A, Metha M. A clinico-pathological study of post coital bleeding. Arch Gynecol and Obstet. 2004270:34-6.

The Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG). College statement C-Gyn 6: Investigation of intermenstrual and postcoital bleeding. [Internet]. RANZCOG 1995 [reviewed 2015 Mar].

Bateson B, Brand A, Hammond I, Mountford J, Whop L, Cancer Council Australia Cervical Cancer Screening Guidelines Working Party. Signs and symptoms of cervical cancer – identification and investigation of abnormal bleeding. [Internet]. 2019. Available from: https://wiki.cancer.org.au/australia/Clinical_question:Investigation_of_abnormal_vaginal_bleeding.

Goldacre M, Loudon N, Watt B, Grant G, Loudon JD, McPherson K, et al. Epidemiology and clinical significance of cervical erosion in women attending a family planning clinic. Br Med J. 19781(6115):748-50.

National Institute for Health and Care Excellence (NICE). Suspected cancer: recognition and referral. Blood and immune system conditions. NG12. [Internet]. NICE 2015 [updated: 2017 Jul]. Available from: https://www.nice.org.uk/guidance/ng12.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-V). 5th ed. Washington DC: APA 2013.

Green L, O’Brien PMS, Panay N, Craig M on behalf of the Royal College of Obstetricians and Gynaecologists. Management of premenstrual syndrome. BJOG. 2017124:e73-e105.

Backstrom T, Heineman K, Nyberg S, Hammarback S. Definition and prevalence of premenstrual syndrome. Gynaecology Forum. 200914:14-7.

Pearlstein T, Bachmann GA, Zacur HA, Yonkers KA. Treatment of premenstrual dysphoric disorder with a new drospirenone-containing oral contraceptive formulation. Contraception. 200572(6):414-21.

Van Die M, Burger HG, Teede HJ, Bone KM. Vitex agnus-castus extracts for female reproductive disorders: a systematic review of clinical trials. Planta Med. 201379:562-75.

Schellenberg R. Treatment for the premenstrual syndrome with agnus castus fruit extract: prospective, randomised, placebo controlled study. BMJ. 2001322(7279):134-7.

Thys-Jacobs S, Starkey P, Bernstein D, Tian J. Calcium carbonate and the premenstrual syndrome: effects on premenstrual and menstrual symptoms. Am J Obstet Gynecol. 1998179(2):442-52.

Brown J, O’Brien PM, Marjoribanks J, Wyatt K. Selective serotonin reuptake inhibitors for premenstrual syndrome. Cochrane Database Syst Rev. 2009Apr 15(2):CD001396.

Green L, O’Brien PMS, Panay N, Craig M on behalf of the Royal College of Obstetricians and Gynaecologists. Green-Top Guideline No. 48: Management of Premenstrual Syndrome. BJOG. 2017124:e73-e105.

eTG Complete. Therapeutic Guidelines 2019. Premenstrual Syndrome.

Whelan A, Jurgens TM, Naylor H. Herbs, vitamins and minerals in the treatment of premenstrual syndrome: a systematic review. Can J Clin Pharmacol. 200916(3):e407-e29.

Wyatt K, Dimmock PW, Jones PW, Shaughn O’Brien PM. Efficacy of vitamin B-6 in the treatment of premenstrual syndrome: systematic review. BMJ. 199922(318).

Quint E, O’Brien RF, AAP the Committee on Adolescence, AAP the North American Society for Pediatric and Adolescent Gynecology. Menstrual Management for Adolescents With Disabilities. Pediatrics. 2016137(4):e20160295.

Kirkman Y, Ornstein M, Aggarwal A, McQuillan S. Menstrual Suppression in Special Circumstances. JOGC. 201941(2):e7-e17.

Wilbur J, Torondel B, Hameed S, Mahon T, Kuper H. Systematic review of menstrual hygiene management requirements, its barriers and strategies for disabled people. PLoS ONE. 201914(2):e210974.

The Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG). College Statement C-Gyn-10: Fertility and menstrual management in women with an intellectual disability. [Internet]. RANZCOG 1997 (reviewed: 2016 Mar). Available from: https://ranzcog.edu.au/RANZCOG_SITE/media/RANZCOG-MEDIA/Women%27s%20Health/Statement%20and%20guidelines/Clinical%20-%20Gynaecology/Fertility-and-menstrual-management-in-women-with-an-intellectual-disability-(C-Gyn-10)-Review-July-2016_1.pdf?ext=.pdf.

Williams C, Creighton S. Menstrual Disorders in Adolescents: Review of current practice. Horm Res Paediatr. 201278:135-43.

Mooed S, Mellor A. Dysmenorrhoea in Adolescents. O&G Magazine. 201719(3).

Velayuthum V, Dahiya R. Disorders of pubertal timing in young people. Medicine Today. 201718(5):24-32.

Abitbol L, Zborovski S, Palmert M. Evaluation of delayed puberty: what diagnostic tests should be performed in the seemingly otherwise well adolescent? Arch Dis Child. 2016101:767-71.

Matthews K, Benny P. Uterine and related structural anomalies. O&G Magazine. 201012(3).

Short A. Congenital anomalies of the female genital tract. O&G Magazine. 201719(3).

Dietrich J, Millar DM, Quint EH. Non-obstructive Müllerian Anomalies. Journal of Pediatric and Adolescent Gynecology. 201427:386-95.