The goals of patient evaluation, are to assess the likely cause of the erectile dysfunction and identify medical or psychologic conditions that may be contributing to the dysfunction or that may influence treatment options. Often one can get an excellent clue to the etiology by the history and physical examination which can then be tested by precise laboratory tests.
History and Clinical ExaminationAnatomic, psychogenic, endocrinologic, neurologic, and vascular abnormalities may all contribute to impotence. A thorough history is the most important factor in the evaluation of the patient with erectile dysfunction. Psychogenic disorders may occasionally be primary factors contributing to erectile dysfunction. Once a concern with the patient's sexual function is identified, the next step is to differentiate erectile dysfunction from other sexual problems, such as loss of libido or ejaculatory problems. The full 15 question IIEF which helps in distinguishing what type of sexual dysfunction is present can be accessed here.
The shortened 5 question IIEF which helps in judging the severity of true erectile dysfunction can be accessed here. Early recognition of psychogenic disturbances allows the physician to avoid costly and confusing evaluation for other etiologies of impotence. Because impotence is known to be associated with many common medical conditions and medications, a careful medical history may yield insights into the etiology of impotence.
Careful physical examination with particular attention to sexual and genital development may occasionally reveal an obvious cause of impotence.
The cardiovascular examination should include assessment of vital signs (especially blood pressure and pulse) and signs of hypertensive or ischemic heart disease. In many cases, a careful history and physical exam will direct the physician to the most expedient cost-effective evaluation and eliminate the need for unnecessary diagnostic tests. Diabetes mellitus: A Cardiovascular Disease Diabetes alone, without co morbid coronary heart disease (CHD), exposes individuals to the same high risk (>20%) as does prior CHD for a major cardiovascular event (cardiovascular risk equivalent).
Diabetes mellitus: A Cardiovascular Disease CVD is a major cause of morbidity, mortality for those with diabetes.
Diabetes mellitus & Hypertension twice Hypertension is twice as common in persons with diabetes as it is in the general populations.
Diabetes mellitus & Hypertension Truncal obesity, hypertension,, insulin resistance, and dyslipidemia are among the components of the metabolic syndrome, which has been associated with an increased risk of coronary heart disease. Beta-Blockers early Increased insulin resistance and a higher incidence of new-onset diabetes mellitus were reported in early trials with beta-blockers. Beta-Blockers not Existing diabetes mellitus is not a contra- indication to beta-blockade, although b1- selective agents are preferable in insulin- dependent patients, to avoid masking hypoglycaemia. Beta-Blockers Patients with diabetes and concomitant CHF or CAD are among those who can benefit most from beta-blockers. COPERNICUS Study advanced HF equivalently In the Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) study of carvedilol, in patients with advanced HF, all- cause mortality was reduced equivalently in diabetic and nondiabetic patients.
Women who have undergone a hysterectomy with oophorectomy are likely to be testosterone deficient.
These changes in hormone levels and tissue integrity occur in a predictable manner with menopause and aging but remain highly variable from woman to woman, and from decade to decade.
Dennerstein and colleagues36 reported similar findings for vaginal dryness with 50% of the women in their Longitudinal Melbourne Mid-Life Study exhibiting vaginal dryness at 3 years postmenopause. Lastly, lubrication, classically thought to be estrogen dependent is actually partly estrogen dependent and partly androgen dependent. High concentrations of estrogen and testosterone are found in the brain, particularly in the hypothalamus and preoptic areas. Observational and clinical trial studies have shown an impact of estrogen and estrogen plus androgen replacement on mood, hot flashes, desire, arousal, and frequency of coitus. Estrogen replacement versus placebo after surgical or natural menopause has been examined by a number of authors. Another set of trials with the same inclusion criteria examined the effect of testosterone therapy in the estrogen replete woman.
The terms drive, libido, desire, and arousal have been used in various ways with some overlap in the literature.
In order to attribute current sexual problems to the changes experienced with menopause, the clinician should confirm that the sexual problems are new in origin, are not caused by an untoward medical condition, and that the woman previously experienced good sexual functioning prior to her menopause. The differential diagnosis could be conceived in terms of central sexual as well as central nonsexual symptoms impacting basic drive. Some premenopausal women have operationally defined sexual problems, though not all are distressed by these problems. Is there a relationship between perimenopausal reproductive function and the onset of mood disorders?
A potential relationship exists between the onset of affective disorders in women and the reproductive events of the perimenopause. While it is important to distinguish between the perimenopause and postmenopause, many older studies failed to do so. Prior to publication of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition,3 several investigators performed more systematic examinations of mood disorders occurring in association with midlife and reproductive senescence.These studies were unable to confirm the existence of involutional melancholia (ie, melancholia occurring in old age), nor were they able to identify epidemiologic evidence for an increased prevalence of major depressive disorder (MDD) during the perimenopause. The presupposition that perimenopause-related affective syndromes are melancholic depressions is an additional confound that may have interfered with the identification and characterization of other affective syndromes (eg, atypical depression) occurring at this time. The menopause has been defined as the permanent cessation of menstruation resulting from loss of ovarian activity.
The perimenopause has been defined as the transitional period from reproductive to nonreproductive life.9,10 As the perimenopause progresses, ovarian follicular depletion occurs, the ovary becomes less sensitive to gonadotropin stimulation, and a state of relative hypoestrogenism occurs. Not only is there evidence suggesting the importance of distinguishing between peri- and postmenopausal women with respect to treatment response characteristics, but studies have also identified that the perimenopause has distinct endocrine subphases, with the early perimenopause (eg, high gonadotropin levels and increased estradiol secretion) differing from the late perimenopause (eg, high gonadotropin levels and decreased estradiol secretion).12,13 Thus, investigators have attempted to develop criteria to define the phases of reproductive senescence.
Similarly, community-based surveys24,25 of the prevalence of affective syndromes (conditions meeting standardized diagnostic criteria) have observed patterns of morbidity consistent with those reported in the surveys examining mood symptoms. There is also evidence that anxiety disorders, although less common than depressive disorders, are experienced by a considerable number of perimenopausal women27 and that the frequency of episodes may increase during the perimenopause (Ellen Freeman, MD, oral communication, 2003). In summary, epidemiological studies examining the prevalence of both affective symptoms and syndromes have documented that the majority of postmenopausal women do not experience a MDD associated with this phase of life.
Several new methodological issues have emerged reflecting, in part, efforts to reconcile substantial differences in the results of observational studies and RCTs of hormone replacement therapy (HRT).
A differential response to estradiol in depression was reported by Appleby and colleagues29 and Montgomery and colleagues,30 with perimenopausal but not postmenopausal women responding to estrogen therapy under RCT conditions. The evidence that younger perimenopausal but not older postmenopausal women respond to estrogen therapy suggests that those mood disorders occurring in perimenopausal women are caused by changes in hormones (eg, withdrawal or fluctuations) rather than prolonged sex steroid deficiency. Investigations of plasma levels of gonadal steroids in women with perimenopause-related depression have identified no consistent abnormality of reproductive endocrine function that distinguishes this disorder. Controlled studies employing synthetic forms of estrogen in the treatment of depression have yielded mixed results. Schmidt and colleagues31 examined the therapeutic efficacy of estradiol replacement in 34 women (approximately 50% of whom had no prior history of depression) with perimenopausal depression under double-blind, placebo-controlled conditions. These findings are consistent with data from Montgomery and colleagues31 and Saletu and colleagues55 suggesting the beneficial effects of estrogen on mood in perimenopausal women reporting depressive symptoms. The decision to prescribe estradiol for perimenopausal depression must further be informed by associated risks and the availability of alternative treatments (such as DHEA, phytoestrogen, or testosterone supplementation). In addition to the possible antidepressant efficacy of estrogen in perimenopausal depression, some but not all63 studies have suggested that the response of peri- (Soares and colleagues, oral communication, 2001) and postmenopausal women64,65 to some antidepressants (ie, SSRIs) may be enhanced by the use of estrogen replacement. Alternative hormonal treatment strategies include DHEA available over-the-counter, phytoestrogens, selective estrogen receptor modulators (SERMs), and testosterone supplementation. The relationship between the onset of depressive illness and reproductive senescence has been a source of controversy. At the same time, some have multiple causes, such as a person with diabetes who is also on certain antihypertensive medications.
Therefore, the evaluation of impotence begins with a comprehensive history and physical examination. Recognition of these patient characteristics should lead the clinician to entertain the possibility of a primary psychogenic etiology of impotence.
The physician should use appropriate vocabulary, avoiding slang or excessively technical terminology. Moreover, many patients complain of erectile dysfunction when they mean something lese such as premature ejaculation etc., and again this needs to be recognized before embarking on the detailed evaluation. Particular attention should be given to the cardiovascular, neurologic and genitourinary systems, as these systems are directly involved with erectile function. Careful examination of the penis may reveal an anatomic abnormality such as a micropenis, the presence of chordee, or a Peyronie's plaque. Abdominal or femoral artery bruits and asymmetric or absent lower extremity pulses are indicative of vascular disease.
Patients with diabetes or neurodegenerative disorders may show evidence of peripheral neuropathy. Use of Beta-Blockers In patients With Diabetes Mellitus Professor Taalat Abd El-Aatty Diabetes & Metabolism Alexandria University. At age 45, approximately 40% of patients with type 2 diabetes also have hypertension, increasing to 60% by age 75.
However, more modern agents such as bisoprolol and carvedilol appear to have no detrimental effect on glucose metabolism.
European guidelines recommend ?-blockers for all diabetic patients with acute cardiac syndrome, post-MI, and in CHF.
Large-scale meta-analyses of available data confirm that major antihypertensive drug classes, (diuretics, ACE inhibitors, calcium antagonists, angiotensin receptor antagonists, and b-blockers) do not differ significantly for their overall ability to reduce BP in hypertension. Alexander is a partner with the Permanente Medical Group of Northern California, and has two voluntary professional positions, executive director of the Alexander Foundation for Women’s Health, a non-profit organization, in Berkeley, and adjunct assistant clinical professor of psychiatry at Stanford Medical School in Palo Alto, both in California.
A portion of this work was begun with an unrestricted educational grant from Solvay to the Kaiser Foundation Research Institute. Changes in circulating levels of estrogen and androgens during the peri- and postmenopausal years have a far-reaching impact on sexual symptoms in some women. The key to the differential diagnosis and treatment of the symptomatic woman is to understand the balance of factors that have resulted in a deterioration of the sexual function to which she has become accustomed. The prevalence rates for specific sexual problems examined in these studies were quite different, depending on the study methodology used.


Desire, drive, arousal, and vulvovaginal health appear to be affected by the neuroendocrine changes that occur with menopause and aging. After menopause, the primary source of estrogen production, the ovaries, cease to produce estrogen. Loss of testosterone is also iatrogenically induced by treatment with exogenous oral estrogen (oral contraception or oral postmenopausal hormone therapy) or chronic glucocorticosteroid therapy causing adrenal suppression.
Research on desire and arousal does indicate an association between clinical symptoms (in the absence of interpersonal or psychiatric etiology) and lower levels of gonadal hormones.
Testosterone concentration is much greater than estrogen concentration in these sites, corresponding to high aromatase activity in these regions.46,47 Androgens may act directly on the brain, or their action may be due to estrogen that has been aromatized from testosterone. Many of these studies do not reflect the entire postmenopausal population; instead, they reflect populations of women who appear to be symptomatic and benefit from this intervention. These trials either eliminated women with hot flashes or analyzed them the impact of hot flashes on sexual dysfunction.
The criteria for whom to give such a therapy, the benefits of peripheral versus systemic, and what kind of peripheral or systemic therapies are most beneficial for different women is beyond the scope of this article. When moving beyond a pure biological model one can begin to look at drive, libido, and the capacity for arousal as being driven by motivation, expectations, and interpersonal, psychological, and contextual variables.17,18 It is the dynamic interaction of these variables that result in sexual activity when a woman is presented with an opportunity for sexual activity. Despite the unresolved issues in the field, enough is known that some clinical recommendations can be made regarding differential diagnosis and treatment of the portion of postmenopausal women who present with sexual functioning problems. Next, the clinician should differentiate the influence of neuroendocrine change from those of psychosocial, interpersonal, and psychological factors. With aging, a woman has the possibility of many changes in the pelvic region, some of which may affect her sexual response and comfort with coital relations. Many postmenopausal women are free of sexual problems for a significant number of years after menopause, prior to the onset of effects of aging on their sexuality.
Report of the international consensus development conference on female sexual dysfunction: definitions and classifications. Sexual problems: a study of the prevalence and need for health care in the general population. Schmidt is chief of the Unit on Reproductive Endocrine Studies in the Behavioral Endocrinology Branch at the National Institute of Mental Health. The perimenopause is a time of considerable variability in reproductive function and, in some women, is associated with an increased susceptibility to depression. For simplicity, this article will use the term perimenopausal depression to refer to depression that presents at the end of reproductive life.
Nonetheless, a debate ensued in the psychiatric literature regarding the nature of these mood and behavioral disturbances and their connection to reproductive aging.
Thus, the earlier debate over the appropriate classification of involutional melancholia changed to skepticism about its existence as a distinct condition. Several authors have described differences between women with perimenopausal versus premenopausal depressions. In fact, as described below, both historical and recent reports of mood disorders during the perimenopause are more consistent with a neurasthenia or minor depression. These criteria will facilitate the collection of more homogeneous samples, aiding understanding of the interaction between the stage of ovarian decline, aging, and a variety of physiological endpoints. On the other hand, several community-based and clinic-based surveys suggest that the perimenopause is relevant to the development of affective disorders26-28 and that a substantial number of perimenopausal women do, in fact, experience a clinically significant affective syndrome. These issues comprise several explanations for differential responses of both behavioral and physiologic measures to changes in hormones (either endogenous or exogenous) across individuals, including phase of reproductive senescence (ie, late perimenopause or early menopause versus 5 years past last menses), presence of menopausal symptoms, the duration of hypogonadism prior to receiving HRT, and genetic polymorphisms that underlie differences in steroid responsivity. These observations were confirmed by several recent RCTs employing standardized psychiatric diagnostic interviews to establish the presence of depression.31-33 Similarly, a literature review and meta-analysis by Yaffe and colleagues34 concluded that the benefits of HRT on cognitive function were limited to perimenopausal women compared with postmenopausal women and suggested that the beneficial effects of HRT were secondary to the concurrent improvement in menopausal symptoms.
The possibility that it is the change or acute withdrawal from ovarian steroids that is relevant in the pathophysiology of these conditions suggests several mechanisms that may be involved in the onset of mood disorders.
After 3 weeks of estradiol, depression rating scale scores were significantly decreased compared to baseline scores and significantly lower than scores in the women receiving placebo. Reproductive status may be characterized by serial plasma FSH or estradiol levels to confirm the presence of the perimenopause and to track improvements in mood if they occur in relation to changes in pituitary-ovarian hormone secretion.
Consequently, if not otherwise contraindicated, estrogen augmentation may be of value in the treatment of perimenopausal depressed women who ostensibly are antidepressant nonresponders. Epidemiologic and clinic-based studies that have distinguished between perimenopause (a time of considerable variability in ovarian hormone secretion) and postmenopause (a time when hormonal changes have long since stabilized) have suggested that in some middle-aged women perimenopause is associated with an increased vulnerability to depression. Involuntional melancholia: an etiologic clinical and social study of endogenous depression in later life, with special reference to genetic factors. A careful sexual history and knowledge of concurrent illnesses and medications are essential. Having the patient define the terms in his own words will help the physician and patient communicate more effectively. Many common medications such as psychotropic drugs and antihypertensives have been associated with impotence. Many factors influence whether or not a woman experiences a symptom and whether or not she finds it distressful. With this information the clinician may focus efforts on the avenues of treatment that have the highest probability of re-establishing the woman’s pre-existing level of sexual functioning. One must also take into account that mood, general health, context, beliefs, and expectations17,18 affect each woman irrespective of her gonadal hormone status. The presence of estrogen in the circulation of postmenopausal women is a function of the conversion of androgens to estrogens at local tissue sites via aromatase activity and then leaking back into circulation. Women who have undergone unilateral or bilateral oophorectomy have lower ovarian androgen production than women who have not had these procedures26 and are likely to be testosterone deficient.
The inclusion criteria were characterized by no previous or current psychiatric problems, no situational stressors, and a stable unconflicted relationship. The choices for local vulvovaginal estrogen would be cream, a twice-weekly vaginal tablet (ie, estradiol vaginal tablets), or an estradiol vaginal ring worn like a diaphragm that releases estrogen over a 3-month period. These would include a decrease in sexual thoughts and fantasies, receptivity, initiation, relevancy, sexual activity, and frequency of coitus. These would include clitoral sensitivity, sensation-sensory perception, lubrication, pain with sexual activity, pelvic vasocongestion, capacity to develop muscle tension, and postcoital bleeding.
Behavioral or cognitive therapy can be considered for problems that appear to be behavioral in origin.
Biological and psychosocial factors affecting sexual functioning during the menopausal transition.
Substitution of an SSRI with bupropion sustained release following SSRI-induced sexual dysfunction. Twenty-four-hour mean plasma testosterone concentration declines with age in normal premenopausal women. A prospective longitudinal study of serum testosterone, dehydroepiandrosterone sulfate, and sex hormone-binding globulin levels through the menopause transition. Marked decline in serum concentrations of adrenal C19 sex steroid precursors and conjugated androgen metabolites during aging. Subnormal plasma dehydroisoandrosterone to cortisol ratio in anorexia nervosa: a second hormonal parameter of ontogenic regression.
Hysterectomy, oophorectomy, and endogenous sex hormone levels in older women: the Rancho Bernardo Study. Effects of hormone replacement therapy on sexual psychophysiology and behavior in postmenopause. Menstrual rhythms in sensory processes: a review of fluctuations in vision, olfaction, audition, taste, and touch. Effects of oestrogen treatment on the size of receptive field and response threshold of pudendal nerve in the female rat. Role of androgens in female genital sexual arousal: receptor expression, structure, and function. Physiological and subjective sexual arousal in pre- and postmenopausal women and postmenopausal women taking replacement therapy.
Ovarian hormones and vaginal blood flow: using laser Doppler velocimetry to measure effects in a clinical trial of post-menopausal women. Induction of vaginal mucification in rats with testosterone and 17b-hydroxy-5a-androstan-3-one.
Vaginal mucification in the ovariectomized rat in response to 5a-pregnane-3,20-dione, testosterone and 5a-androstan-17b-ol-3-one: test for progestogenic activity.
Estradiol and testosterone in specific regions of the human female brain in different endocrine states. Quality of life of postmenopausal women on a regimen of transdermal estradiol therapy: a double-blind placebo-controlled study. Effects of estrogen, androgen, and progestin on sexual psychophysiology and behavior in postmenopausal women. Estrogen and estrogen-androgen replacement in postmenopausal women dissatisfied with estrogen-only therapy.
Testosterone enhances estradiol’s effects on postmenopausal bone density and sexuality.
Changes in sexual behavior as a function of plasma sex steroid levels in post-menopausal women. Comparative effects of oral esterified estrogens with and without methyltestosterone on endocrine profiles and dimensions of sexual function in postmenopausal women with hypoactive sexual desire.
Effect of combined implants of oestradiol and testosterone on libido in postmenopausal women. Transdermal testosterone treatment in women with impaired sexual function after oophorectomy [see comments]. Addition of testosterone to estrogen replacement therapy in oophorectomized women: effects on sexuality and well-being. The effects of oral contraceptives on mood and sexuality: a comparison of triphasic and combined preparations. Are our definitions of women’s desire, arousal and sexual pain disorders too broad and our definition of orgasmic disorder too narrow? Female androgen insufficiency: the Princeton consensus statement on definition, classification, and assessment. Rubinow is clinical director and chief in the Behavioral Endocrinology Branch at the National Institute of Mental Health in Bethesda, Maryland.


Whether the variability in ovarian hormone secretion during the perimenopause has any causal role in the development of depression remains unclear. Studies examining the prevalence, presentation, and pathophysiology of mood disorders occurring during the perimenopause are presented as well. Moreover, these findings suggested that hormonal events did not underlie mood disorders occurring during midlife and reproductive senescence. Stenstedt4 and Brown and colleagues5 both reported involutional-onset depression to be associated with a lower family history of depression than that observed in patients with early-onset depression.
The levels of several other hormones that may also impact on mood and behavior decrease with aging concomitant with changes in reproductive function.
For example, the Stages of Reproductive Aging Workshop criteria for reproductive, perimenopausal (menopausal transition), and postmenopausal years developed by Soules and colleagues17 define the early perimenopause to include women with menstrual cycle irregularity (defined as a variable cycle length that differs from normal by more than 7 days) and elevated plasma FSH secretion.
In contrast, a recent multisite study by Weissman and colleagues24 identified an increased hazard rate for the onset of depression in the cohort of women (but not men) 45–50 years of age. Thus, estradiol treatment may be effective for panic attacks; however, it is unclear if this improvement is secondary to relief of hot flashes (which may trigger as well as mimic panic attacks) or due to the direct effects of estradiol on panic disorder. A subsequent meta-analysis of a similar literature performed by LeBlanc35 confirmed Yaffe’s suggestion and observed that the presence of symptoms (eg, hot flashes, sleep disturbance, or mood disturbance) predicted a beneficial effect of HRT on cognition. Additionally, several adequate treatments for depression exist, and, therefore, the first-line medication for perimenopausal women presenting with depression is a traditional antidepressant, such as an SSRI.
As in other types of depression, psychotherapy is an important adjunct to pharmacologic or hormonal interventions and can prove crucial in women for whom the menopause holds negative meaning (eg, a hysterectomy can be a traumatic loss for some women) and in those who have significant life stressors and poor social supports.
Additional support for this suggestion is provided by double-blind RCTs documenting the therapeutic efficacy of estradiol in perimenopausal depressed women but not in postmenopausal depressed women. The endocrinology of the menopausal transition: a cross-sectional study of a population-based sample. Potentially predictive and manipulable blood serum correlates of aging in the healthy human male: progressive decreases in bioavailable testosterone, dehydroepiandrosterone sulfate, and the ratio of insulin-like growth factor 1 to growth hormone.
Circulating levels of growth hormone, insulin- like growth factor-I and growth hormone binding protein in normal women of advanced reproductive age. The relative contributions of endocrine changes and social circumstances to depression in mid-aged women. Sex and depression in the National Comorbidity Survey I: lifetime prevalence, chronicity and recurrence. Effect of oestrogen and testosterone implants on psychological disorders in the climacteric. Efficacy of estradiol for the treatment of depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial.
Lack of efficacy of estradiol for depression in postmenopausal women: a randomized controlled trial. Hormone replacement therapy and incidence of Alzheimer disease in older women: the Cache County study. Long-term treatment with estrogen and progesterone enhances acquisition of a spatial memory task by ovariectomized aged rats. The sexual history should include the duration of impotence, level of libido, and a complete inventory of sexual partners.
The International Index of Erectile Function (IIEF) is a valuable tool for defining the area of sexual dysfunction.
Similarly, a patient's surgical history may also provide clues to the possible causes of impotence. Certain genetic syndromes such as Kallmann's or Klinefelter's syndrome may present with obvious physical signs of hypogonadism or distinctive body habitus. The superficial anal reflex, indicative of normal somatic function of sacral cord levels S24, is assessed by touching the perianal skin and noting contraction of the external anal sphincter muscles. 3.Are ?-blockers the first line treatment for control of hypertension in patients with diabetes? In CHF studies, ?-blockers have consistently shown a significant benefit in patients with diabetes.
3.Are ?-blockers the first life treatment for control of hypertension in patients with diabetes? Alexander’s time was supported by the Northern California Permanente Medical Group Psychiatry Model of Care Program. Postmenopausal women have been reported to have the symptoms of a peripheral neuropathy characterized by numbness, itching, clothing intolerance, and increased two-point discrimination thresholds.35 The untreated clinical consequences of these physiologic changes secondary to hypoestrogenemia can be dyspareunia, vulvovaginal atrophy, and delayed or decreased orgasm, and the genital and extragenital symptoms listed above.
She may have maintained sexual activity under the same influences when she was younger but postmenopausally, the change in gonadal hormones along with those same influences may have led to a change in her desire or libido.
Central nonsexual would include mood-dysphoria, motivation, energy, fatigue, vitality, well-being, and hot flashes affecting libido indirectly. This group of women may present for care, which will require a full knowledge of the biological as well as the interpersonal, psychosocial, and psychological domains affecting their sexuality by the treating clinicians. Rubinow is a consultant to Servier and Vela, and has received research support from Watson. Recent epidemiologic data confirm that the perimenopause is a time of increased susceptibility to the onset of depression. Finally, recommendations on the clinical evaluation and management of these conditions are provided. A study by Weissman6 demonstrated that the percentage of women with first-onset depression was higher in perimenopausal and postmenopausal women than in younger women; the increased years at risk for depression in the older women would have suggested the contrary. During the late perimenopause there is a continued elevation of FSH in conjunction with two or more skipped cycles and a period of amenorrhea lasting ≥60 days. Moreover, hot flashes and panic improve after treatment with selective serotonin reuptake inhibitors (SSRIs), suggesting a potential shared pathophysiology as well as treatment response characteristics. These data suggest that estrogen’s effect on depression is not solely a product of its ability to reduce the distress of hot flushes.
These data emphasize that the stage of reproductive senescence may predict response to estrogen, as originally reported by Appleby and colleagues.29 Thus, perimenopausal women who are undergoing changes in reproductive function may be more responsive to estrogen than postmenopausal women, whose hormonal changes have long since stabilized. Indeed, recent reports documenting the therapeutic benefits of SSRIs in hot flashes support a more prominent role for these medications in the management of perimenopausal depression. However, progestin-induced dysphorias are not uniformly experienced in all women, nor are predictors of the dysphoric response known. The IIEF is designed to be a self-administered measure of erectile dysfunction, but it also assesses a patient's function in other phases of sexual function. Prior radical pelvic surgery (eg, prostatectomy, abdominoperineal resection), radiation, and pelvic trauma are known to be associated with impotence. For those women who do experience sexual symptoms, and where these symptoms can be attributed to reduced levels of gonadal hormones, the use of estrogen or estrogen plus testosterone replacement therapy can be successful in improving sexual function. However, some postmenopausal women may exceed this level, depending upon quantity of adipose tissue as well as other factors.
Systemic estrogen therapies would include different oral estrogens with different pharmacologic compositions and half lives, patches or injections, and gels.
For many cases a dual approach is warranted where the gynecologist or family practitioner replaces to the lowest necessary level of estrogen either peripherally or peripherally (local) and centrally (systemic) and observes for biological improvement concurrent with mental health interventions. A successful intervention for these women will require shared knowledge between specialties and more cooperation among specialties for successful outcomes.
Additionally, although similar to major depressive disorder in phenomenology, course, and family and personal history of mood disorder, perimenopausal depression may be distinguished by an antidepressant response to estradiol therapy. Thus, while perimenopausal MDDs do not appear to be phenomenologically distinct, evidence suggests that they may differ from earlier-onset depressions with respect to family history and age of first depressive episode. This could include up to 1 year of amenorrhea, at which time the woman has entered the early stages of postmenopause. Thus, progestins should not be contraindicated in the presence of an antidepressant response to estradiol in a depressed perimenopausal woman (and are advised in women with a uterus). The IIEF also establishes a reliable baseline that can be used to monitor changes related to treatment. It is performed by placing a finger in the rectum and noting contraction of the anal sphincter and bulbocavernosus muscle when the glans penis is squeezed. Davis is associate professor in the Department of Epidemiology and Preventive Medicine, Monash Medical Center in Melbourne and director of research at the Jean Hailes Foundation in Clayton, both in Australia. However, it is important to recognize that in addition to this biologic etiology of new-onset sexual symptoms in the postmenopausal woman, several nonbiologic domains influence sexual functioning as well.
Testosterone systemic therapy is limited at this time to a combined pill of estrogen and methyltestosterone, estratest half-strength and estratest, and two products currently under phase II and III trials, a testosterone gel and a testosterone patch. Schmidt is a consultant to Zynx and has received material support from TAP pharmaceuticals and Watson. This article presents background information relevant to the controversy surrounding the putative relationship between reproductive aging and mood disorders, reviews the endocrinology of the perimenopause, and describes several emerging methodologic issues that may help reconcile conflicting findings in past observational studies and recent randomized controlled trials. Further, epidemiological and even phenomenological similarity does not entail causal identity. These data, therefore, provide additional evidence supporting the role of the perimenopause, but not the postmenopause, in the development of mood disorders.
While estradiol treatment is no longer appropriate for prophylaxis, it is still reasonably prescribed for acute symptoms and syndromes, including depression.
These domains could be thought of as being interpersonal, sociocultural or psychosocial, and psychological in nature. There are other forms of delivery that have been used outside the United States, such as injectables, but are not promoted inside the US. Studies examining the prevalence, presentation, and treatment response characteristics of mood disorders occurring during the perimenopause are described as well. It is not unusual in medicine for phenomenologically similar disorders to have different precipitants or causes. The article concludes with recommendations for the evaluation and treatment of women with perimenopausal depression.
For example, meningitis in both the neonate and infant may present with fever, vomiting, and drowsiness, yet different pathogenic organisms are typically involved with each age group.



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