Abstract
Before considering the various symptoms potentially attributable to the ‘menopause’, let us define the terminology.
Before considering the various symptoms potentially attributable to the ‘menopause’, let us define the terminology.
Whilst ‘menopause’ means the ‘end of menstruation’, ‘menopausal symptoms’ refer to a number of different symptoms associated with the climacteric, the transition from mature reproductive function, through the perimenopause to no ovarian follicular function. The hormonal changes leading up to this stage commence several years earlier, and this period is called the ‘perimenopause’ or ‘menopausal transition’.
Postmenopause is the period a woman enters once she has not menstruated for at least 12 months. The symptoms, which then persist for life, are due to the ovary not producing estrogen any longer, and thus reflect a permanent hormone deficiency syndrome, that of hypoestrogenism.
The physiological basis of these changes relates to the changes in a woman’s ability to regularly ovulate (Chapter 1). Normal ovulation is the culmination of a complex interaction between the various elements of the hypothalamo–pituitary–ovarian axis. Loss of regulation of these complex hormonal changes results in the loss of a predictable cycle at this time and is associated with widely fluctuating levels of estrogen and the development of menopausal symptoms.
Before the menopausal transition, estrogen and progesterone circulate throughout the body, and have many different effects on various systems, some of which we do not necessarily understand as yet. The development of the Graafian follicles with maturation of the oocyte, ovulation and then subsequent formation of the corpus luteum is a complex process. Should any component of the menstrual cycle not function properly, there will be changing levels of circulating hormones, which can have deleterious effects.
A woman has about 400 000 potential oocytes in the ovary at menarche, and she loses these at a rate of about 1000 per month. This is not influenced by taking the combined oral contraceptive pill, which, although it inhibits ovulation, does not spare oocytes. It is well recognized that with aging, there are less and less potential oocytes, and less effective ovulation. Therefore, frequently ovulatory cycles have a deficient corpus luteum function, with lower levels and/or a shortened period of progesterone secretion, and many cycles are anovulatory with no progesterone secreted at all. The consequent imbalance in estrogen and progesterone is thought to be responsible for some of the symptoms during the perimenopause, especially those associated with menstrual problems. Once a woman becomes postmenopausal, ovarian function ceases completely, and the symptoms of the postmenopause relate to an estrogen deficiency syndrome. This chapter focuses on the menopausal transition, also known as the climacteric.
As these symptoms and signs are usually reported as a continuum, we usually consider them together, and classify them into several types:
1. Vasomotor: these include ‘hot flushes’, palpitations, night sweats and altered sleep pattern and fatigue.
2. Neuromuscular: these include headaches and joint and muscle pain. Other degenerative changes may occur such as hair and skin changes, which can include a crawling sensation (formication) and itchy skin.
3. Psychogenic: these include poor concentration, forgetfulness, depression, anxiety, claustrophobia, agoraphobia, irritability, difficulty coping and tearfulness and lack of drive including sex drive.
4. Urogenital: symptoms of vaginal dryness, utero-vaginal prolapse and urinary symptoms of urge incontinence/overactive bladder. Although stress incontinence is more common in postmenopausal women, the aetiology of this is probably not due to estrogen deficiency but disruption of the pelvic diaphragm so that the proximal urethra becomes extra abdominal, and a pressure gradient develops when there is raised intra-abdominal pressure.
5. Indirect symptoms of menopausal osteoporosis: which may result in repeated fractures, especially the wrist and hip.
There is huge variation in the frequency and severity of menopausal symptoms between different women. About 20 per cent of women have no significant symptoms, 60 per cent have mild to moderate symptoms and 20 per cent have very severe symptoms.
Women who have a sudden menopause induced by surgery (oophorectomy) or chemo/radiotherapy usually have more severe symptoms.
Vasomotor Symptoms
These are the classic symptoms heralding the onset of the menopause. About 75 per cent of women in the US report experiencing troublesome flushes – or flashes as they are called in the US [1]. Hot flushes adversely affect the quality of life and the day-to-day functioning of many women during the ‘perimenopause’. Data on the duration of these symptoms are available from the Melbourne Women’s Midlife Health Project [2]. The researchers found that out of 205 women who never used hormone replacement therapy (HRT) and were followed up for 13 years the mean duration of troublesome symptoms was 5.2 years (median 4 years and standard deviation of 3.8 years). Interestingly, even in women who used HRT (total sample 438 women) the duration did not change, with a mean of 5.5 years (median of 4 years, standard deviation of 4.0 years).
Thus it appears that vasomotor symptoms in a cross section of women on average persist for about 5 years.
The Mechanism of Hot Flushes
The basic physiological mechanism for hot flushes is an activation of the heat dissipation response most likely due to a hypothalamic mechanism triggered by decreasing estrogen levels [1]. It is thought that estrogen deprivation results in a loss of negative feedback for hypothalamic noradrenaline synthesis [3].
Peripheral changes that result in altered vascular activity, and a narrowed thermoneutral zone, have also been implicated [4]. Consequently, fluctuations in temperature that would not normally trigger vasodilatation and sweating (cooling-down mechanisms) result in inappropriate flushing due to narrowing of the thermoneutral zone. Women suffering from hot flushes lose the ability to respond to an ice stimulus with vasoconstriction. It is thought likely that the α-adrenergic system, specifically noradrenaline, is the chemical trigger.
Flushes can be aggravated by stress and anxiety, and even by diet, lifestyle and medications.
The intensity of hot flushes can be measured by the increase in finger blood flow, respiratory exchange ratio, core body temperature and skin temperature changes. In laboratory studies, sternal skin conductance is usually measured with good reproducibility [1].
Although night sweats can keep women awake at night, insomnia associated with the menopause is likely to be due to a separate mechanism (loss of neuronal modulation of energy metabolism), and one can occur without the other [5].
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