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Endocrinology and physiology of pseudocyesis
Reproductive Biology and Endocrinology volume 11, Article number: 39 (2013)
This literature review on pseudocyesis or false pregnancy aims to find epidemiological, psychiatric/psychologic, gynecological and endocrine traits associated with this condition in order to propose neuroendocrine/endocrine mechanisms leading to the emergence of pseudocyetic traits. Ten women from 5 selected studies were analyzed after applying stringent criteria to discriminate between cases of true pseudocyesis (pseudocyesis vera) versus delusional, simulated or erroneous pseudocyesis. The analysis of the reviewed studies evidenced that pseudocyesis shares many endocrine traits with both polycystic ovarian syndrome and major depressive disorder, although the endocrine traits are more akin to polycystic ovarian syndrome than to major depressive disorder. Data support the notion that pseudocyetic women may have increased sympathetic nervous system activity, dysfunction of central nervous system catecholaminergic pathways and decreased steroid feedback inhibition of gonadotropin-releasing hormone. Although other neuroendocrine/endocrine pathways may be involved, the neuroendocrine/endocrine mechanisms proposed in this review may lead to the development of pseudocyetic traits including hypomenorrhea or amenorrhea, galactorrhea, diurnal and/or nocturnal hyperprolactinemia, abdominal distension and apparent fetal movements and labor pains at the expected date of delivery.
According to the fifth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-5) , pseudocyesis [from the Greek words pseudes (false) and kyesis (pregnancy); a.k.a. false, imaginary, simulated, phantom, hysterical or spurious pregnancy] is a rare disorder with characteristic somatic features. It is included in the Not Elsewhere Classified section of Somatic Symptom Disorders, a group of disorders that typically present first in non-psychiatric settings characterized predominantly by somatic symptoms or concerns that are associated with significant distress and/or dysfunction. The fact that it is included in a Not Elsewhere Classified section means that it is in a category by itself, different from other Somatic Symptom Disorders such as Functional Neurological Disorder (previously, Conversion Disorder).
Pseudocyesis is defined by the DSM-5 as a false belief of being pregnant that is associated with objective signs and reported symptoms of pregnancy, which may include abdominal enlargement, reduced menstrual flow, amenorrhea, subjective sensation of fetal movement, nausea, breast engorgement and secretions, and labor pains at the expected date of delivery.
Cases of pseudocyesis nowadays are found more frequently in rural undeveloped countries where women usually are not examined by a physician or a midwife until they are in labor or seek medical aid [2, 3]. In developed countries, women visit obstetricians in the first trimester of pregnancy who have more accurate means of diagnosis including pregnancy tests and ultrasonographic examinations. These diagnostic procedures may help pseudocyetic women to be convinced of their non-pregnant condition, that usually leads to resolution of pseudocyesis within minutes or even seconds. Furthermore, women from developed countries in general are more educated and sophisticated, and their emotional conflicts result in a more profound, refined mode of expression than that of pseudocyesis (cited by Pawlowski and Pawlowski ).
Table 1 shows the incidence of pseudocyesis registered in several USA and African hospitals. The relative high incidence of pseudocyesis found in these studies, except for Boston Hospitals , is likely due to the importance that most African black cultures give to fertility together with low educational background [3, 6] and sterility problems [5, 7]. For instance, in the Igbo culture of southeast Nigeria, married women wish to become pregnant because pregnancy and childbirth confirm womanhood and secure the woman’s place in her husband family. This societal pressure may precipitate pseudocyesis as a psychological defense to intense stress if the woman proves to be infertile . Recently, it has been reported that African-American women perceive higher average social messages to have children than White women (social messages were assessed in a national random-digit dial telephone survey via two items: it is important to my partner that we have children; and it is important to my parents that I have children) .
We should emphasize that the definition of pseudocyesis contrasts with delusion of pregnancy, deceptive or simulated pregnancy and erroneous pseudocyesis (for review, see O’Grady and Rosenthal ). Delusion of pregnancy is a Somatic Type (i.e., delusion that the individual has some general medical condition) Delusional Disorder classified by the DSM-5 within Schizophrenia Spectrum and Other Psychotic Disorders. It refers to the false belief of being pregnant in the absence of physical sings suggestive of pregnancy that may be experienced by psychotic women [10–12] and men [13, 14]. According to the DSM-5, the disorder is not a consequence of the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition. Although at first glance it appears that it is easy to distinguish between true pseudocyesis (pseudocyesis vera) and delusion of pregnancy, sometimes delusions of pregnancy present along with physical traits of pseudocyesis [15–18] making difficult to perform a differential diagnosis.
A deceptive or simulated pregnancy is a Factitious Disorder Imposed on Self classified by the DSM-5 within the category of Somatic Symptom Disorders. In this case, the woman acknowledges being pregnant knowing that it is not true ([19, 20]; for review, see O’Grady and Rosenthal ).
Finally, erroneous pseudocyesis refers to cases when the woman erroneously misinterprets symptoms suggestive of pregnancy, including amenorrhea, galactorrhea and/or abdominal enlargement, resulting from either organic diseases (e.g., hormone-secreting tumor [21–23], alcoholic liver disease , cholecystitis , urinary tract infection complicated by urine retention ) or exposure to a substance (e.g., a medication [27–30]).
Whereas most studies have presented pseudocyesis cases as medical curiosities, a few studies have focused their attention on ascertaining the neuroendocrine/endocrine mechanism underlying this condition. These studies, however, have not reported consistent changes in plasma levels of prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), estradiol (E2), progesterone (P) and testosterone (T) (for reviews, see Small  and O’Grady and Rosenthal ). The lack of consistency among studies is not at all surprising if we take into account the small sample sizes and the different endocrine methodologies (e.g., different blood sampling frequency or type of assay for measuring hormones) used in these studies, as well as the ambiguous or null psychiatric/psychologic and/or diagnostic criteria applied to define and discriminate between cases of pseudocyesis vera versus delusional, simulated or erroneous pseudocyesis.
In this review, we aim to find epidemiological, psychiatric/psychologic, gynecological and endocrine traits associated with pseudocyesis vera in order to propose neuroendocrine/endocrine mechanisms leading to the development of pseudocyetic traits.
A review of the current and older literature on studies on human pseudocyesis was performed. The review was based on publications up to January 2013 identified by PubMed database searches using the following key words: pseudocyesis and women. In addition, a hand search was done to explore the references cited in the primary articles. Only studies in which women met the DSM-5 definition of pseudocyesis (see above) and provided clear evidence that women did not suffer from simulated or erroneous pseudocyesis were selected for entering into the study. Furthermore, in order to exclude cases of delusion of pregnancy and focus exclusively on pseudocyesis vera, only studies in which a psychiatric/psychologic evaluation provided proof that women were non-psychotic were included in the study (Table 2). Two exceptions, however, were allowed: (1) a woman that refused psychiatric evaluation but her hormonal responses to thyroid-stimulating hormone (TRH) stimulation and dexamethasone suppression tests were similar to those seen in major depressive disorders . This woman was entered into the study because most (8 out of 10 women) of the pseudocyetic women included in Table 2 suffered from mild to major depression; and (2) an unidentified member of a cohort of 5 women that was not psychologically evaluated for unreported reasons . This woman was included in Table 2 because the potential bias that her inclusion may introduce in the analysis, if the woman suffered from delusion of pregnancy, is relatively small. In Table 3 we provide data from the studies excluded from the study that did not meet the inclusion criteria.
The chronological age of pseudocyetic women included in Table 2 ranged from 16 to 39 years. Eight women suffered from mild to major depression, one woman was not psychologically evaluated for unreported reasons  and another did not meet the criteria for depression disorder but exhibited a histrionic and hypochondriac personality . As the majority of the pseudocyetic women suffered from mild to major depression and 3 [32–35] out of the 5 studies suggested that the endocrinological traits of pseudocyetic women resemble those of polycystic ovarian syndrome (PCOS), data from pseudocyetic women were qualitatively compared with those reported for PCOS and major depressive disorder.
PCOS is a heterogeneous disease characterized by hyperandrogenemia (predominantly of ovarian origin: the ovaries produce up to 60% of androgens, while the remaining 40% is of adrenal origin), hirsutism, oligo- or amenorrhea and anovulation, and is frequently associated with hyperinsulinemia, insulin resistance syndrome, increased cardiovascular risk and diabetes mellitus (for reviews, see McCartney et al. , Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group  and Burt Solorzano et al. ). Note as well that there are many subgroups of depression differing from each other in their neuroendocrine/endocrine traits. Thus, for the sake of homogeneity, we chose the well-characterized major depressive disorder group as a reference group.
It is important to mention that the studies included in Table 2 used different endocrine methodologies (e.g., different blood sampling frequency or type of assay for measuring hormones). For this reason, the absolute hormonal concentrations reported in these studies cannot be compared among studies. Instead, Table 2 and Table 3 provide the authors’ original terminology that was used to describe whether hormonal levels were “elevated”, “low” or “within normal range” when compared to control data from either the own authors’ laboratory [33, 34] or from other contemporary sources [16, 32, 35].
Similarities and differences among pseudocyesis, PCOS and major depressive disorder
Table 4 shows a summary of the traits that characterize pseudocyesis, PCOS and major depressive disorder according to the variables included in Table 2. The comparative analysis shows that pseudocyetic women share many endocrine traits with PCOS and major depressive disorder, although these traits are more akin to PCOS than to major depressive disorder. Note that the fact that pseudocyetic women share many endocrine traits with PCOS does not necessarily mean that pseudocyetic women suffer from PCOS (we are not aware of any study reporting the presence of polycystic ovaries in pseudocyetic women). As mentioned above, pseudocyesis is a psychiatric condition. It is not a consequence of either organic diseases (including PCOS) or exposure to a substance.
Neuroendocrine/endocrine pathways of pseudocyesis
Most pseudocyetic women suffer from mild to major depression, anxiety and/or emotional stress due to psychologic conflicts or needs, such as women who simultaneously wish for children and fear becoming pregnant (for reviews, see Small , O’Grady and Rosenthal  and Whelan and Stewart ) or women who have an overwhelming desire to become pregnant because of societal pressures [3, 7]. In this context, we should mention that patients with major depression have a deficit in brain dopamine and norepinephrine activity , and increased sympathetic nervous system activity associated with a higher rate of entry to plasma of norepinephrine released from sympathetic nerves (norepinephrine spillover rate) [90, 91] and elevated plasma levels of norepinephrine . In rodents, chronic psychosocial stress is also associated with reduced brain dopamine and norepinephrine activity and elevated plasma levels of norepinephrine (for reviews, see Goddard et al.  and Rasheed and Alghasham ). PCOS women also show low dopamine hypothalamic tone (for review, see Hernández et al. ).
Data from the present review indicate that pseudocyetic women may have a deficit in brain dopamine activity. This fact supports the notion that pseudocyetic women may have a dysfunction of central nervous system catecholaminergic pathways involved in the regulation of anterior pituitary hormone secretion. Dopamine  and norepinephrine  have been recently identified in mice as potent steroid-independent inhibitors of gonadotropin-releasing hormone (GnRH) neuron excitability and firing. Moreover, dopamine in women inhibits pulsatile LH (for review, see Jaffe et al. ) and PRL (for review, see Ben-Jonathan and Hnasko ) secretion. Thus, a deficit/dysfunction in brain catecholaminergic activity may result in increased pulsatile GnRH, LH and PRL and an elevated LH/FSH ratio. These endocrine changes may induce hypomenorrhea or amenorrhea, galactorrhea and diurnal and/or nocturnal hyperprolactinemia - traits found in most pseudocyetic women. Also, the reduced brain catecholaminergic activity displayed by pseudocyetic women may combine/interact with a drop in steroid feedback inhibition of GnRH. In particular, the relatively high levels of T found in pseudocyetic women may decrease GnRH sensitivity to P feedback inhibition resulting in increased GnRH pulse frequency, elevated LH pulsatility and higher LH production over FSH such as occurs in PCOS women (for reviews, see McCartney et al.  and Burt-Solorzano et al. ). Finally, the increased sympathetic nervous system activity likely shown by pseudocyetic women may be implicated, not only in the apparent fetal movements and labor pains at the expected date of delivery felt by some pseudocyetic women, but also in the typical abdominal enlargement displayed by most pseudocyetic women.
Several authors have proposed a mixture of causes to explain the physiological mechanism by which abdominal swelling takes place in pseudocyetic women. This mixture of causes includes chronic contraction of the diaphragmatic muscle (this contraction pushes the bowel downward in the abdominal cavity), assumption of a lordotic posture, increased omental and abdominal wall fat, and mild to marked constipation and/or bowel distention (for reviews, see Small , O’Grady and Rosenthal  and Whelan and Stewart ). However, the distended abdomen, that may remain bloated for months immediately (within minutes or even seconds) disappears, with or without release of flatus, after pseudocyetic women are convinced of their non-pregnant state or under anesthesia. This observation indicates that although increased omental and abdominal wall fat, and mild to marked constipation and/or bowel distention may contribute to abdominal enlargement, they are not primary causes of abdominal protrusion. Furthermore, unlike normal pregnancy, the umbilicus does not become everted, the abdominal distension is uniform and rounded, and the abdominal wall presents a rubbery, tense muscular tone being tympanic on percussion. All these facts point to the diaphragm and/or certain groups of muscles of the abdominal wall as the primary cause of abdominal enlargement. In particular, pseudocyetic women may experience chronic contraction of the diaphragm accompanied by abnormal patterns of contraction/relaxation of the anterior abdominal and internal oblique muscles. This mechanism, called abdomino-phrenic dyssynergia, has been observed in patients with abdominal bloating and distension after colonic-gas-load-induced abdominal distension . Interestingly, literature shows cases of persistent  or spasmodic (spasms resembling those of a woman in labor ) hysterical abdominal proptosis likely resulting from abdomino-phrenic dyssynergia.
It is worth mentioning that, in contrast to normal individuals that can push out the abdominal wall only for a relatively short period of time even in the presence of the quietest respiration, persistent hysterical abdominal proptosis is unaffected by a cough or by a sneeze, nor by emptying the bladder or by straining at stool . However, it disappears after relaxing the patient’s diaphragm by having the patient take a deep inspiration followed by a sudden expiration or by having the patient hold her/his breath as long as possible such as occurs in pseudocyesis (for reviews, see Alvarez  and O’Grady and Rosenthal ).
Importantly, the 2 phrenic nerves that originate in the neck (mainly from the 4th cervical nerve, but which also receive contributions from the 5th and 3rd cervical nerves) and pass down between the lung and heart to reach the diaphragm, contain not only motor fibers but also proprioceptive and sympathetic fibers to the diaphragm, and sensory fibers to the pleura and pericardium. Therefore, dysfunction of the sympathetic nervous system in pseudocyetic women, mediated directly via impulses transmitted through the sympathetic nervous system and/or indirectly via plasma norepinephrine released from sympathetic nerves or secreted from the adrenal medulla, may induce abdomino-phrenic dyssynergia resulting in abdominal protrusion.
In this literature review, we have analyzed epidemiological, psychiatric/psychologic, gynecological and endocrine traits of 10 pseudocyetic women reported in 5 selected studies after applying stringent criteria to discriminate between cases of pseudocyesis vera versus delusional, simulated or erroneous pseudocyesis. The analysis performed shows that pseudocyetic women share many endocrine traits with PCOS and major depressive disorder, although these traits are more akin to PCOS than to major depressive disorder.
The reviewed data support the notion that pseudocyetic women may have: increased sympathetic nervous system activity; dysfunction of central nervous system catecholaminergic pathways involved in the regulation of hormone secretion from adenohypophysis; and decreased steroid feedback inhibition of GnRH. These neuroendocrine/endocrine disorders may cause hypomenorrhea or amenorrhea, galactorrhea, diurnal and/or nocturnal hyperprolactinemia, abdominal distension and apparent fetal movements and labor pains at the expected date of delivery - traits exhibited by most pseudocyetic women. However, other neuroendocrine/endocrine pathways not yet analyzed in pseudocyetic women may also be involved in the development of pseudocyetic traits. These may include, the hypothalamic-pituitary-adrenal axis; neurotransmitters controlling GnRH neuron excitability ; and dopamine stimulators and inhibitors of PRL secretion (for review, see Ben-Jonathan and Hnasko ).
Free androgen index
Follicle stimulating hormone
Polycystic ovarian syndrome
Standard error of the mean
Somatotropin release-inhibiting factor
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 2013, Washinton, DC: APA, in preparation for publication in May 2013, 5
Pawlowski EJ, Pawlowski MM: Unconscious and abortive aspects of pseudocyesis. Wis Med J. 1958, 57: 437-540.
Ouj U: Pseudocyesis in a rural southeast Nigerian community. J Obstet Gynaecol Res. 2009, 35: 660-665. 10.1111/j.1447-0756.2008.00997.x.
Cohen LM: A current perspective of pseudocyesis. Am J Psychiatr. 1982, 139: 1140-1144.
Fried PH, Rakoff AE, Schopbach RR, Kaplan AJ: Pseudocyesis; a psychosomatic study in gynecology. J Am Med Assoc. 1951, 145: 1329-1335. 10.1001/jama.1951.02920350023005.
Brenner BN: Pseudocyesis in Blacks. S Afr Med J. 1976, 50: 1757-1759.
Dafallah SE: Pseudocyesis and infertility. Saudi Med J. 2004, 25: 964-965.
Mcquillan J, Greil AL, Shreffler KM, Wonch-Hill PA, Gentzler KC, Hathcoat JD: Does the reason matter? variations in childlessness concerns among U.S. women. J Marriage Fam. 2012, 74: 1166-1181.
O’Grady JP, Rosenthal M: Pseudocyesis: a modern perspective on an old disorder. Obstet Gynecol Surv. 1989, 44: 500-511. 10.1097/00006254-198907000-00003.
Brooks JG: Pseudocyesis in a 6-year-old girl: follow-up report at 23. J Am Acad Child Psychiatr. 1985, 24: 359-362. 10.1016/S0002-7138(09)61099-2.
Milner GL, Hayes GD: Pseudocyesis associated with folie à deux. Br J Psychiatr. 1990, 156: 438-440. 10.1192/bjp.156.3.438.
Harland RF, Warner NJ: Delusions of pregnancy in the elderly. Int J Geriatr Psychiatr. 1997, 12: 115-117. 10.1002/(SICI)1099-1166(199701)12:1<115::AID-GPS486>3.0.CO;2-L.
Shutty MS, Leadbetter RA: Case report: recurrent pseudocyesis in a male patient with psychosis, intermittent hyponatremia, and polydipsia. Psychosom Med. 1993, 55: 146-148.
Adityanjee AM: Delusion of pregnancy in males: a case report and literature review. Psychopathology. 1995, 28: 307-311. 10.1159/000284942.
Hardwick PJ, Fitzpatrick C: Fear, folie and phantom pregnancy: pseudocyesis in a fifteen-year-old girl. Br J Psychiatr. 1981, 139: 558-560. 10.1192/bjp.139.6.558.
Starkman MN, Marshall JC, La Ferla J, Kelch RP: Pseudocyesis: psychologic and neuroendocrine interrelationships. Psychosom Med. 1985, 47: 46-57.
Hernández-Rodríguez I, Moreno MJ, Morano LE, Benavente JL: Systemic lupus erythematosus presenting as pseudocyesis. Br J Rheumatol. 1994, 33: 400-402. 10.1093/rheumatology/33.4.400.
Ahuja N, Vasudev K, Lloyd A: Hyperprolactinemia and delusion of pregnancy. Psychopathology. 2008, 41: 65-68. 10.1159/000110628.
Posner LB, de Chabert RA, Posner AC: Simulated pregnancy following pseudocyesis. Am J Obstet Gynecol. 1962, 83: 976-977.
Daw E: Pseudocyesis. Br J Clin Pract. 1973, 27: 181-183.
Chambers WR: Brain tumor simulating pregnancy. Am J Obstet Gynecol. 1955, 70: 212-213.
Echániz A, Millán A, del Río Fuentes A, Pedreira JD: Pseudopregnancy and gastric adenocarcinoma. Med Clin (Barc). 1984, 83: 307-308.
Manzi D, Greenberg B, Maier D, Forouhar F, Malchoff CD: Bronchogenic carcinoma presenting as a pseudopregnancy. Chest. 1995, 107: 567-569. 10.1378/chest.107.2.567.
Alfonso CA: Pseudocyesis with concomitant medical illness. Gen Hosp Psychiatr. 1990, 12: 205-206. 10.1016/0163-8343(90)90080-V.
Benzick JM: Illusion or hallucination? Cholecystitis presenting as pseudopregnancy in schizophrenia. Psychosomatics. 2000, 41: 450-452. 10.1176/appi.psy.41.5.450.
Yeh YW, Kuo SC, Chen CY: Urinary tract infection complicated by urine retention presenting as pseudocyesis in a schizophrenic patient. Gen Hosp Psychiatr. 2012, 34: 101.e9-101.e10. 10.1016/j.genhosppsych.2011.06.008.
Flanagan PJ, Harel Z: Pseudocyesis in an adolescent using the long-acting contraceptive Depo-Provera. J Adolesc Health. 1999, 25: 238-240. 10.1016/S1054-139X(99)00021-X.
Ahuja N, Moorhead S, Lloyd AJ, Cole AJ: Antipsychotic-induced hyperprolactinemia and delusion of pregnancy. Psychosomatics. 2008, 49: 163-167. 10.1176/appi.psy.49.2.163.
Manjunatha N, Saddichha S: Delusion of pregnancy associated with antipsychotic induced metabolic syndrome. World J Biol Psychiatr. 2009, 10: 669-670. 10.1080/15622970802505800.
Seeman MV: Antipsychotic-induced amenorrhea. J Ment Health. 2011, 20: 484-491. 10.3109/09638237.2011.586741.
Small G: Pseudocyesis: an overview. Can J Psychiatr. 1986, 31: 452-457.
Ayers JW, Seiler JC: Neuroendocrine indices of depression in pseudocyesis. A case report. J Reprod Med. 1984, 29: 67-70.
Devane GW, Vera MI, Buhi WC, Kalra PS: Opioid peptides in pseudocyesis. Obstet Gynecol. 1985, 65: 183-188.
Yen SS, Rebar RW, Quesenberry W: Pituitary function in pseudocyesis. J Clin Endocrinol Metab. 1976, 43: 132-136. 10.1210/jcem-43-1-132.
Tulandi T, McInnes RA, Mehta A, Tolis G: Pseudocyesis: pituitary function before and after resolution of symptoms. Obstet Gynecol. 1982, 59: 119-121.
McCartney CR, Eagleson CA, Marshall JC: Regulation of gonadotropin secretion: implications for polycystic ovary syndrome. Semin Reprod Med. 2002, 20: 317-326. 10.1055/s-2002-36706.
Rosner W, Auchus RJ, Azziz R, Sluss PM, Raff H: Position statement: Utility, limitations, and pitfalls in measuring testosterone: an Endocrine Society position statement. J Clin Endocrinol Metab. 2007, 92: 405-413.
Massafra C, De Felice C, Agnusdei DP, Gioia D, Bagnoli F: Androgens and osteocalcin during the menstrual cycle. J Clin Endocrinol Metab. 1999, 84: 971-974. 10.1210/jc.84.3.971.
Bui HN, Sluss PM, Blincko S, Knol DL, Blankenstein MA, Heijboer AC: Dynamics of serum testosterone during the menstrual cycle evaluated by daily measurements with an ID-LC-MS/MS method and a 2nd generation automated immunoassay. Steroids. 2013, 78: 96-101. 10.1016/j.steroids.2012.10.010.
Asukai K, Uemura T, Minaguchi H: Occult hyperprolactinemia in infertile women. Fertil Steril. 1993, 60: 423-427.
Bouilly J, Sonigo C, Auffret J, Gibori G, Binart N: Prolactin signaling mechanisms in ovary. Mol Cell Endocrinol. 2012, 356: 80-87. 10.1016/j.mce.2011.05.004.
Maes M, Van Gastel A, Blockx P, Martin M, Cosyns P, Scharpé S, Desnyder R: An augmented escape of androstenedione from suppression by dexamethasone in melancholia: relationships to intact ACTH and cortisol nonsuppression. J Affect Disord. 1995, 34: 291-300. 10.1016/0165-0327(95)00027-K.
Maeda K, Kato Y, Ohgo S, Chihara K, Yoshimoto Y, Yamaguchi N, Kuromaru S, Imura H: Growth hormone and prolactin release after injection of thyrotropin-releasing hormone in patients with depression. J Clin Endocrinol Metab. 1975, 40: 501-505. 10.1210/jcem-40-3-501.
Extein I, Pottash AL, Gold MS, Silver JM: Thyroid-stimulating hormone response to thyrotropin-releasing hormone in unipolar depression before and after clinical improvement. Psychiatr Res. 1982, 6: 161-169. 10.1016/0165-1781(82)90004-X.
Arita H, Kinoshita M, Oshino S, Kitamura T, Otsuki M, Kasayama S, Shimokawa T, Shimomura I, Yoshimine T, Saitoh Y: Biological characteristics of growth hormone-producing pituitary adenomas are different according to responsiveness to thyrotropin-releasing hormone. J Clin Endocrinol Metab. 2012, 97: 2741-2747. 10.1210/jc.2012-1125.
Kaltsas T, Pontikides N, Krassas GE, Seferiadis K, Lolis D, Messinis IE: Growth hormone response to thyrotrophin releasing hormone in women with polycystic ovarian syndrome. Hum Reprod. 1999, 14: 2704-2708. 10.1093/humrep/14.11.2704.
Chihara K, Kashio Y, Kita T, Okimura Y, Kaji H, Abe H, Fujita T: L-dopa stimulates release of hypothalamic growth hormone-releasing hormone in humans. J Clin Endocrinol Metab. 1986, 62: 466-473. 10.1210/jcem-62-3-466.
Ben-Jonathan N, Hnasko R: Dopamine as a prolactin (PRL) inhibitor. Endocr Rev. 2001, 22: 724-763. 10.1210/er.22.6.724.
Spiliotis BE: Growth hormone insufficiency and its impact on ovarian function. Ann N Y Acad Sci. 2003, 997: 77-84. 10.1196/annals.1290.009.
Yen SS, Quigley ME, Reid RL, Ropert JF, Cetel NS: Neuroendocrinology of opioid peptides and their role in the control of gonadotropin and prolactin secretion. Am J Obstet Gynecol. 1985, 152: 485-493.
Hugues JN, Theron-Gerard L, Coussieu C, Pasquier M, Dewailly D, Cedrin-Durnerin I: Assessment of theca cell function prior to controlled ovarian stimulation: the predictive value of serum basal/stimulated steroid levels. Hum Reprod. 2010, 25: 228-234. 10.1093/humrep/dep378.
Zarate A, Canales ES, Soria J, Jacobs LS, Daughaday WH, Kastin AJ, Schally AV: Gonadotropin and prolactin secretion in human pseudocyesis: effect of synthetic luteinizing hormone-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH). Ann Endocrinol (Paris). 1974, 35: 445-450.
Osotimehin BO, Ladipo OA, Adejuwon CA, Otolorin EO: Pituitary and placental hormone levels in pseudocyesis. Int J Gynaecol Obstet. 1981, 19: 399-402. 10.1016/0020-7292(81)90024-2.
Tulandi T, McInnes RA, Lal S: Altered pituitary hormone secretion in patients with pseudocyesis. Fertil Steril. 1983, 40: 637-641.
Forsbach G, Güitron A, Munoz M, Bustos H: Pituitary function in human pseudocyesis. J Endocrinol Invest. 1987, 10: 39-43.
Bray MA, Muneyyirci-Delale O, Kofinas GD, Reyes FI: Circadian, ultradian, and episodic gonadotropin and prolactin secretion in human pseudocyesis. Acta Endocrinol (Copenh). 1991, 124: 501-509.
Padayachi T, Ashe R, Moodley J, Jialal I: Pituitary function tests in black patients with pseudocyesis. S Afr Med J. 1991, 79: 24-26.
Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group: Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril. 2004, 81: 19-25.
Burt-Solorzano CM, Beller JP, Abshire MY, Collins JS, McCartney CR, Marshall JC: Neuroendocrine dysfunction in polycystic ovary syndrome. Steroids. 2012, 77: 332-337. 10.1016/j.steroids.2011.12.007.
Williams KE, Marsh WK, Rasgon NL: Mood disorders and fertility in women: a critical review of the literature and implications for future research. Hum Reprod Update. 2007, 13: 607-616. 10.1093/humupd/dmm019.
Legro RS, Schlaff WD, Diamond MP, Coutifaris C, Casson PR, Brzyski RG, Christman GM, Trussell JC, Krawetz SA, Snyder PJ, Ohl D, Carson SA, Steinkampf MP, Carr BR, McGovern PG, Cataldo NA, Gosman GG, Nestler JE, Myers ER, Santoro N, Eisenberg E, Zhang M, Zhang H, Reproductive Medicine Network: Total testosterone assays in women with polycystic ovary syndrome: precision and correlation with hirsutism. J Clin Endocrinol Metab. 2010, 95: 5305-5313. 10.1210/jc.2010-1123.
Baischer W, Koinig G, Hartmann B, Huber J, Langer G: Hypothalamic-pituitary-gonadal axis in depressed premenopausal women: elevated blood testosterone concentrations compared to normal controls. Psychoneuroendocrinology. 1995, 20: 553-559. 10.1016/0306-4530(94)00081-K.
Laven JS, Imani B, Eijkemans MJ, Fauser BC: New approach to polycystic ovary syndrome and other forms of anovulatory infertility. Obstet Gynecol Surv. 2002, 57: 755-767. 10.1097/00006254-200211000-00022.
Hardoy MC, Serra M, Carta MG, Contu P, Pisu MG, Biggio G: Increased neuroactive steroid concentrations in women with bipolar disorder or major depressive disorder. J Clin Psychopharmacol. 2006, 26: 379-384. 10.1097/01.jcp.0000229483.52955.ec.
Kaltsas T, Pontikides N, Krassas GE, Seferiadis K, Lolis D, Messinis IE: Effect of gonadotrophin-releasing hormone agonist treatment on growth hormone secretion in women with polycystic ovarian syndrome. Hum Reprod. 1998, 13: 22-26. 10.1093/humrep/13.1.22.
Jarrett DB, Kupfer DJ, Miewald JM, Grochocinski VJ, Franz B: Sleep-related growth hormone secretion is persistently suppressed in women with recurrent depression: a preliminary longitudinal analysis. J Psychiatr Res. 1994, 28: 211-223. 10.1016/0022-3956(94)90007-8.
Yildiz BO, Azziz R: The adrenal and polycystic ovary syndrome. Rev Endocr Metab Disord. 2007, 8: 331-342. 10.1007/s11154-007-9054-0.
Kurita H, Maeshima H, Kida S, Matsuzaka H, Shimano T, Nakano Y, Baba H, Suzuki T, Arai H: Serum dehydroepiandrosterone (DHEA) and DHEA-sulfate (S) levels in medicated patients with major depressive disorder compared with controls. J Affect Disord. 2013, 146 (2): 205-212. 10.1016/j.jad.2012.09.004.
Herbert J: Cortisol and depression: three questions for psychiatry. Psychol Med. 2012, 8: 1-21.
Polson DW, Reed MJ, Scanlon MJ, Quiney N, Franks S: Androstenedione concentrations following dexamethasone suppression: correlation with clomiphene responsiveness in women with polycystic ovary syndrome. Gynecol Endocrinol. 1988, 2: 257-264. 10.3109/09513599809029350.
Lewandowski KC, Cajdler-Łuba A, Salata I, Bieńkiewicz M, Lewiński A: The utility of the gonadotrophin releasing hormone (GnRH) test in the diagnosis of polycystic ovary syndrome (PCOS). Endokrynol Pol. 2011, 62: 120-128.
Acar B, Kadanali S: Diminished growth hormone responses to L-dopa in polycystic ovarian disease. Fertil Steril. 1993, 60: 984-987.
Lee EJ, Lee BS, Lee HC, Park KH, Song CH, Huh KB: Growth hormone response to L-dopa and pyridostigmine in women with polycystic ovarian syndrome. Fertil Steril. 1993, 60: 53-57.
McPherson H, Walsh A, Silverstone T: Growth hormone and prolactin response to apomorphine in bipolar and unipolar depression. J Affect Disord. 2003, 76: 121-125. 10.1016/S0165-0327(02)00077-0.
Ansseau M, Von Frenckell R, Cerfontaine JL, Papart P, Franck G, Timsit-Berthier M, Geenen V, Legros JJ: Blunted response of growth hormone to clonidine and apomorphine in endogenous depression. Br J Psychiatr. 1988, 153: 65-71. 10.1192/bjp.153.1.65.
Pitchot W, Ansseau M, Gonzalez Moreno A, Hansenne M, von Frenckell R: Dopaminergic function in panic disorder: comparison with major and minor depression. Biol Psychiatr. 1992, 32: 1004-1011. 10.1016/0006-3223(92)90061-4.
Pitchot W, Hansenne M, Gonzalez Moreno A, Ansseau M: Growth hormone response to apomorphine in panic disorder: comparison with major depression and normal controls. Eur Arch Psychiatr Clin Neurosci. 1995, 245: 306-308. 10.1007/BF02191872.
Barnes RB, Lobo RA: Central opioid activity in polycystic ovary syndrome with and without dopaminergic modulation. J Clin Endocrinol Metab. 1985, 61: 779-782. 10.1210/jcem-61-4-779.
Blank SK, McCartney CR, Marshall JC: The origins and sequelae of abnormal neuroendocrine function in polycystic ovary syndrome. Hum Reprod Update. 2006, 12: 351-361. 10.1093/humupd/dml017.
Martín del Campo AF, Dowson JH, Herbert J, Paykel ES: Diurnal variations in endocrine and psychological responses to 0.2 mg/kg naloxone administration in patients with major depressive disorder and matched controls. J Affect Disord. 2000, 57: 37-47. 10.1016/S0165-0327(99)00070-1.
Wortsman J, Hirschowitz JS: Galactorrhea and hyperprolactinemia during treatment of polycystic ovary syndrome. Obstet Gynecol. 1980, 55: 460-463.
Swaab DF, Bao AM, Lucassen PJ: The stress system in the human brain in depression and neurodegeneration. Ageing Res Rev. 2005, 4: 141-194. 10.1016/j.arr.2005.03.003.
Bao AM, Ji YF, Van Someren EJ, Hofman MA, Liu RY, Zhou JN: Diurnal rhythms of free estradiol and cortisol during the normal menstrual cycle in women with major depression. Horm Behav. 2004, 45: 93-102. 10.1016/j.yhbeh.2003.09.004.
Anderson RA, Groome NP, Baird DT: Inhibin A and inhibin B in women with polycystic ovarian syndrome during treatment with FSH to induce mono-ovulation. Clin Endocrinol (Oxf). 1998, 48: 577-584. 10.1046/j.1365-2265.1998.00442.x.
Fraser IS, Kovacs G: Current recommendations for the diagnostic evaluation and follow-up of patients presenting with symptomatic polycystic ovary syndrome. Best Pract Res Clin Obstet Gynaecol. 2004, 18: 813-823.
Burgers JA, Fong SL, Louwers YV, Valkenburg O, de Jong FH, Fauser BC, Laven JS: Oligoovulatory and anovulatory cycles in women with polycystic ovary syndrome (PCOS): what's the difference?. J Clin Endocrinol Metab. 2010, 95: E485-E489. 10.1210/jc.2009-2717.
Machado-Vieira R, Zarate CA: Proof of concept trials in bipolar disorder and major depressive disorder: a translational perspective in the search for improved treatments. Depress Anxiety. 2011, 28: 267-281. 10.1002/da.20800.
Whelan CI, Stewart DE: Pseudocyesis–a review and report of six cases. Int J Psychiatr Med. 1990, 20: 97-108. 10.2190/XBTE-XBKX-3HKA-8W89.
Lambert G, Johansson M, Agren H, Friberg P: Reduced brain norepinephrine and dopamine release in treatment-refractory depressive illness: evidence in support of the catecholamine hypothesis of mood disorders. Arch Gen Psychiatr. 2000, 57: 787-793. 10.1001/archpsyc.57.8.787.
Esler M, Turbott J, Schwarz R, Leonard P, Bobik A, Skews H, Jackman G: The peripheral kinetics of norepinephrine in depressive illness. Arch Gen Psychiatr. 1982, 39: 295-300. 10.1001/archpsyc.1982.04290030035006.
Veith RC, Lewis N, Linares OA, Barnes RF, Raskind MA, Villacres EC, Murburg MM, Ashleigh EA, Castillo S, Peskind ER, Pascuali M, Halter JB: Sympathetic nervous system activity in major depression. Basal and desipramine-induced alterations in plasma norepinephrine kinetics. Arch Gen Psychiatr. 1994, 51: 411-422. 10.1001/archpsyc.1994.03950050071008.
Roy A, Pickar D, Linnoila M, Potter WZ: Plasma norepinephrine level in affective disorders. Relationship to melancholia. Arch Gen Psychiatr. 1985, 42: 1181-1185. 10.1001/archpsyc.1985.01790350055010.
Goddard AW, Ball SG, Martinez J, Robinson MJ, Yang CR, Russell JM, Shekhar A: Current perspectives of the roles of the central norepinephrine system in anxiety and depression. Depress Anxiety. 2010, 27: 339-350. 10.1002/da.20642.
Rasheed N, Alghasham A: Central dopaminergic system and its implications in stress-mediated neurological disorders and gastric ulcers: short review. Adv Pharmacol Sci. 2012, 2012: 182671-
Hernández I, Parra A, Méndez I, Cabrera V, Cravioto MC, Mercado M, Díaz-Sánchez V, Larrea F: Hypothalamic dopaminergic tone and prolactin bioactivity in women with polycystic ovary syndrome. Arch Med Res. 2000, 31: 216-222. 10.1016/S0188-4409(00)00059-X.
Liu X, Herbison AE: Dopamine regulation of gonadotropin-releasing hormone neuron excitability in male and female mice. Endocrinology. 2013, 154: 340-350. 10.1210/en.2012-1602.
Han SK, Herbison AE: Norepinephrine suppresses gonadotropin-releasing hormone neuron excitability in the adult mouse. Endocrinology. 2008, 149: 1129-1135.
Jaffe RB, Plosker S, Marshall L, Martin MC: Neuromodulatory regulation of gonadotropin-releasing hormone pulsatile discharge in women. Am J Obstet Gynecol. 1990, 163: 1727-1731. 10.1016/0002-9378(90)91436-G.
Villoria A, Azpiroz F, Burri E, Cisternas D, Soldevilla A, Malagelada JR: Abdomino-phrenic dyssynergia in patients with abdominal bloating and distension. Am J Gastroenterol. 2011, 106: 815-819. 10.1038/ajg.2010.408.
Ewing MR, Millar JH: Hysterical abdominal proptosis; records of a case. Br Med J. 1955, 2: 1124-1125. 10.1136/bmj.2.4948.1124.
Lerner MA: Hysterical abdominal proptosis. Am J Roentgenol Radium Ther Nucl Med. 1974, 122: 275-277. 10.2214/ajr.122.2.275.
Alvarez WC: Hysterical type of nongaseous abdominal bloating. Arch Intern Med (Chic). 1949, 84: 217-245. 10.1001/archinte.1949.00230020020002.
We thank the contribution of a native English speaking scientist (Dr. ST) for carefully proofreading and correcting the manuscript for grammar and spelling mistakes. This study was supported by PS09/00136 from Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación, cofinanced by the Fondo Europeo de Desarrollo Regional (FEDER).
The authors declare that they have no competing interests.
JJT was involved in the conception and design of the study, the acquisition, analysis and interpretation of data and drafting of the article. CH, MAGP and AC were involved in the analysis and interpretation of data, and revising the article critically for important intellectual content. All authors read and approved the final manuscript.
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Tarín, J.J., Hermenegildo, C., García-Pérez, M.A. et al. Endocrinology and physiology of pseudocyesis. Reprod Biol Endocrinol 11, 39 (2013). https://doi.org/10.1186/1477-7827-11-39
- Hypothalamus-pituitary-ovarian axis
- Major depression disorder
- Polycystic ovarian syndrome
- Sympathetic nervous system