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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women tend to suffer more often from migraine than men (19% vs. 9%). Further menstruation is associated with attacks in 60% of women who have migraine. Moreover 14% of women with migraine suffer from attacks only with menses. Migraine may be linked to late luteal phase dysphoric disorder and dysmenorrhea. these conditions occur when the greatest fluctuation of estrogen levels occur. These fluctuations indeed cause prostaglandin levels to rise, prolactin release to intensify, and central nervous system opioid dysregulation to occur. In fact, several studies show that decreasing levels of estrogen activate menstrual migraine. Further estrogens and progesterone trigger synthesis of endometrial prostaglandins. In fact, prostaglandins regulate descending norepinephrine pain control systems in the brain, thus increased levels of prostaglandins decreases the pain threshold. In addition, falling levels of estrogens produce dopamine receptor hypersensitivity. Dopamine antagonists cause increased prolactin release throughout the luteal phase in all women and during the entire menstrual cycle in women with menstrual migraine. Physicians can treat menstrual migraine with various nonsteroidal antiinflammatory drugs, simple or combination analgesics, ergotamine, or hormonal therapy when other treatments fail. They should be aware that diuretics and pyridoxine are ineffective in treating menstrual migraine. Several replacement therapies to treat menopausal women with migraine exist. these include adding androgens, reducing estrogen dosage, converting to continuous dosing, and converting to parenteral dosing. Some data show an increase in or severity of migraine among oral contraceptive (OC) users, but other studies find no difference in headache among OC and placebo users. In fact, OCs may exacerbate, improve, or not change the frequency or severity of headaches.
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PMID:The role of sex hormones in headache. 155 90

Some pituitary hormones secrete hormones while others do not. Nonsecreting tumors can interfere with normal pituitary hormone secretion and produce tumor symptoms and signs like headaches and visual field defects. The most frequent hormone-secreting tumors are prolactinomas. Growth hormone or ACTH or gonadotropin or gonadotropin-alpha and beta chain-producing tumors are less frequent, TSH producing tumors are extremely rare. The most important elements of the diagnostic work-up are clinical signs and symptoms, assessment of pituitary function (measurement of TSH, free T4, LH, FSH, oestradiol/free testosteron, growth hormone, IGF-1, prolactin, ACTH, Cortisol, serum and urine osmolality), CT and/or MRI and, in patients with large tumors, a visual field exam. The treatment of choice of pituitary tumors is often surgery. Alternative therapies are radiation treatment (in nonoperable patients or when hormone levels are persistently elevated after pituitary surgery) and drug treatment (dopamine agonists in hyperprolactinemia, somatostatin analogues in acromegaly). Pituitary hormone deficiencies are treated depending on the specific deficiency with thyroxine, cortisone, oestrogen/gestagen/testosterone gonadotropines or ADH analogues.
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PMID:[Hypophyseal dysfunction and tumors]. 158 68

The patients was a 27-year-old female, gravida 0, para 0, with complaint of headache and visual disturbance for about 1 month. Ophthalmological examination showed impaired visual acuity and enlargement of Mariotte's spot on the left. A computed tomography scan disclosed an enhanced mass in the sellar and suprasellar region. Endocrinological examination revealed slight elevation of thyroxin, growth hormone, and prolactin. A trans-sphenoidal hypophysectomy was carried out with a preoperative diagnosis of nonfunctioning pituitary adenoma. Histological examination showed a marked infiltration of lymphocytes and interstitial fibrosis, diagnosed as lymphocytic adenohypophysitis. She received hormone-replacement therapy owing to postoperative hypopituitarism. Twenty-eight cases of lymphocytic adenohypophysitis including the author's are classified clinically into two types; fulminant type and chronic type. The former type occurs frequently with disturbance of consciousness because of the end organ insufficiency and proceeds to death in a fulminant course. The latter type occurs frequently with headache and visual disturbances, closely related to pregnancy and the postpartum period and survival occurs with hormone replacement therapy. This disease should be kept in mind in the diagnosis of sellar and suprasellar mass lesions.
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PMID:[Lymphocytic adenohypophysitis. Case report]. 170 64

Cardiac pains related to estrogen therapy for prostatic cancer (PC) emerged in 53% of treated patients with ischemic heart disease (IHD). The pain complaints were associated with impairment of coronary circulation in 48% of cases. This clinical condition is attributed to elevated STH levels and a trend to hypercorticism. In hypertensive PC patients estrogens provoked more frequent and severe headaches which occurred at initial stages of the treatment in 23% and after 1-year administration of hormones in 44% of patients. Hypertensive reactions may be caused by aldosterone and prolactin hyperproduction. Observation of the therapist and endocrinologist can help to prevent complications in IHD patients with PC.
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PMID:[Changes in hormonal homeostasis and development of disorders of the cardiovascular system in patients with prostatic cancer on estrogen therapy]. 172 22

Seventy-three patients with headache underwent serum and cerebrospinal fluid (CSF) radioimmunoassays of follicle-stimulating hormone (FSH), luteinizing hormone (LH), cortisol and prolactin. Serum FSH showed significant increases in all headache patients while serum LH increased only in females. Such a rise of serum FSH and LH is attributed to disturbances of the sleep-wake cycle. On the other hand, serum cortisol was significantly decreased in the male headache patients, probably due to altered circadian rhythm. Serum prolactin remained within normal limits. CSF prolactin, FSH and LH showed detectable levels in all headache sufferers compared to undetectable levels in control subjects, while CSF cortisol was significantly reduced.
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PMID:Hormonal changes in headache patients. 177 42

The goal pursued has been to analyze clinical observations and hormonal studies of patients with empty sella turcica (EST), in order to review this disorder and determine if it can be considered a real syndrome. Fifteen patients with EST (3 men and 12 women) and mean age of 45.6 +/- 17.9 years have been prospectively studied. In the hypothalamus-hypophysis study, reserves of thyrotropin (TSH), prolactin (PRL), gonadotropins (FSH and LH), growth hormone (GH), adrenocorticotropin (ACTH) and cortisol were assessed. In addition, thyroid hormones and, for men, testosterone, were determined. The pathogenic mechanism was explained in two cases (13.3%). We registered headache in 10 patients, obesity in 8, arterial hypertension in 2 and diabetes mellitus in 2. Multiparity antecedent was found in 2 cases. The hormonal study was abnormal in two cases (40%). Most common abnormalities were hyperprolactinemia (3 cases), deficit of gonadotropins (3 cases), without coexisting both of them in any case, and deficit of GH (2 cases). EST is frequently associated with endocrine disfunction, although clinical implications are rare. The absence of common clinical manifestations in most cases questions the EST as a real syndrome.
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PMID:[Primary empty sella turcica: clinical aspects and hormonal study of 15 cases]. 179 Feb 77

From 1962 to 1987, 126 patients underwent trans-sphenoidal surgery for primary treatment of pituitary adenomas unassociated with clinical or biochemical evidence of hormonal overproduction. There were 73 male and 53 female patients (mean age, 50 +/- 12 years). Before surgery, 56% of the patients (70 of 124) had headaches, 74% (94 of 126) had deterioration of vision, and 12% (15 of 126) had ophthalmoplegia. Endocrine evaluation revealed the presence of hypogonadism in 75% (87 of 115), adrenal insufficiency in 36% (46 of 126), and hypothyroidism in 18% (21 of 122). Plasma prolactin was increased in 65% (56 of 86) with a mean level of 39 +/- 14 micrograms/l (normal, 3 to 20 micrograms/l). Radiologic enlargement of the sella turcica was documented in all cases: 67% (84 of 126) had enclosed and 33% (42 of 126) had invasive adenomas. After surgery, vision was normalized or improved in 75% (71 of 94) of the patients. Thyroid, adrenal, and gonadal functions were improved in 14% (three of 22), 41% (19 of 46), 11% (ten of 87), were unchanged in 82% (100 of 122), 77% (97 of 126), 89% (102 of 115), and worsened in 15% (19 of 22), 8% (ten of 126), 3% (102 of 115), respectively. Permanent diabetes insipidus occurred in 5% (seven of 126). Two patients died during the immediate postoperative period. The recurrence rate in patients with a mean follow-up of 6.4 +/- 4.2 years was 21% (15 of 71). These data indicate that trans-sphenoidal microsurgery is an effective and safe initial treatment for patients with nonsecreting pituitary adenoma and may reverse hypopituitarism.
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PMID:The clinical and endocrine outcome to trans-sphenoidal microsurgery of nonsecreting pituitary adenomas. 185 85

Patients previously treated with H2-receptor blocking agents (cimetidine or ranitidine) exhibited a complex neurobehavioral and gastroenteric syndrome, including anxiety, insomnia, anorexia, growing thin, irritability, tachycardia, diarrhoea, nausea, vomiting, abdominal pain, headache, vertigo. These symptoms were dramatically reduced by administration of cimetidine or ranitidine, and reappeared with a new suspension of the therapy. The withdrawal syndrome from H2-receptor antagonists was reversed by treatment with domperidone (10 mg three times per day), a potent hyperprolactinaemic drug which does not cross the blood brain barrier. These results suggest that the drop in prolactin levels that occurs when cimetidine or ranitidine are suspended may contribute to the development of the withdrawal syndrome.
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PMID:[The H2-antagonist therapy withdrawal syndrome: the possible role of hyperprolactinemia]. 198 22

Migraine headaches appear to be linked to the menstrual cycle and the use of oral contraceptives (OCs). Migraine attacks occur during menses in 60% of women and appear to be related to the withdrawal of estrogen. The fluctuations in estrogen levels associated with migraine headaches produce biochemical changes in prostaglandin production, prolactin release, and opoid regulation. Treatment seeks to interrupt the pathophysiological sequence of menstrual-related migraine through the administration of nonsteroidal anti-inflammatory drugs, ergotamine, or, in refractory cases, hormonal agents. The frequency of migraine decreases with age, but tends either to regress or worsen during menopause. In some cases, estrogen replacement therapy for menopausal symptoms produces headache and it may be necessary to reduce the estrogen dose or change from conjugated estrogen to pure estradiol or estrone. The incidence and severity of migraines are also affected by OC use. OCs may trigger migraine episodes and exacerbate or alleviate pre-existing headache. This variable response seems to be a result of individual differences in intrinsic estrogen neuronal response. Although migraine itself may be a risk factor in stroke, there is no evidence that this risk is increased in migrainers who use OCs.
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PMID:Estrogens, progestins, and headache. 204 18

Flunarizine, a calcium antagonist widely used in the prophylactic treatment of migraine, may interfere with dopaminergic systems. Flunarizine therapy can in fact induce extrapyramidal side effects and can increase basal as well as stimulated prolactin levels. To better define the mechanism of flunarizine action in migraine, we studied prolactin and growth hormone responses to thyrotropin releasing hormone and sulpiride in 13 female migraineurs before and after 60 days of flunarizine therapy. The treatment did not modify basal prolactin and growth hormone levels, but prolactin response to thyrotropin releasing hormone was enhanced. A paradoxical increase of growth hormone to thyrotropin releasing hormone observed before therapy was blunted after flunarizine treatment. These data indicate a modulatory action of flunarizine on dopaminergic systems which might to some extent explain the antimigraine action of this drug.
Cephalalgia 1990 Feb
PMID:Possible involvement of dopaminergic mechanisms in the antimigraine action of flunarizine. 210 77


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