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

A 38-year-old woman complained of headache, visual impairment, and diabetes insipidus for 18 months prior to rapid onset of Cushing syndrome and amenorrhea. An autopsy disclosed a pituitary carchinoma invading the right cavernous sinus and two liver metastases. The tumor cells were chromophobic and agranular, with scarce polymorphism and rare mitoses. A review of the literature showed that the association of Cushing syndrome to pituitary carcinomas increases in direct proportion to the occurence of metastases. Such association was noted in almost half of the reported cases of pituitary carcinomas with extracranial dissemination.
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PMID:Pituitary carcinoma with liver metastases and Cushing syndrome. Report of a case. 111 93

Five male patients sought medical attention for diplopia and were found to have third nerve palsies secondary to pituitary adenomas. In four cases this was the only neurologic abnormality. In the fifth there was an additional, asymptomatic, temporal visual field defect in one eye. Partial third nerve involvement was seen in all but one patient. Four patients underwent successful surgery and were found to have chromophobe adenomas. One patient had clinical and laboratory evidence of Cushing's syndrome. An initial diagnosis of cerebral aneurysm was made in three cases when the third nerve palsy followed a severe, acute headache. Later it became evident that pituitary apoplexy was the correct diagnosis. The mechanisms by which a pituitary adenoma causes a third nerve palsy are discussed. The importance of recognizing a pituitary tumor as the etiology of an isolated third nerve palsy is emphasized.
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PMID:Third nerve palsy: the presenting sign of a pituitary adenoma in five patients and the only neurological sign in four patients. 293 21

An unusually therapy-resistant form of Nelson's syndrome developed in a 23-year-old woman two years after treatment of a pituitary-dependent Cushing's syndrome by bilateral adrenalectomy (1977). Removal of a corticotrophic adenoma by a first transsphenoidal pituitary operation (1979) brought only temporary relief. Two years later, regrowth and apoplexy of the pituitary adenoma led to oculomotor paralysis and had to be treated by a second transsphenoidal operation (1981). A second relapse became manifest two years later. Treatment with bromocriptine relieved the headaches but did not diminish the tumor size. A third pituitary operation (1984) became necessary when neurological signs revealed penetration of the cavernous sinus. The tumor was only partly removed by transsphenoidal surgery. Postoperative deterioration of the patient required emergency craniotomy to check a subarachnoidal hemorrhage and for removal of the remaining tumor. The patient died three days later of pneumococcal meningitis which had developed after the third pituitary operation.
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PMID:[A fatal course of Nelson syndrome]. 323 90

The case of a 60-year-old woman with pheochromocytoma and concomitant adrenocortical adenoma in the same gland is presented. She complained of episodic headache, palpitation, nausea, vomiting and sweating. Physical examination revealed that the patient has generalized obesity, wet skin and paroxysmal hypertension, but no signs of Cushing's syndrome. Elevated levels of urinary noradrenaline, adrenaline and total metanephrine were sequentially observed. In addition, urinary 17-OHCS was also slightly elevated, but plasma cortisol was normal and suppressed after oral administration of 0.5 mg of dexamethasone. Abdominal echography and CT scanning demonstrated a left adrenal tumor, which took up both 131I-meta-iodobenzylguanidine and 75Se-scintadoren in the same region. A left adrenalectomy was performed and the tumor was found to consist of two parts, pheochromocytoma (2.5 X 2.5 X 2.5 cm) and cortical adenoma (2.5 X 3 X 5 cm). A total of 23 reported cases showing evidence of hyperfunction of the adrenal cortex and the medulla were noted. So far as we know, this patient was the second case of pheochromocytoma with adrenocortical adenoma in Japan.
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PMID:Pheochromocytoma associated with adrenocortical adenoma: case report and literature review. 372 Jun 79

There is little absolute data in the form of prospective studies in patients with specific illnesses who are on oral contraceptives (OCs). Consequently, the clinician must depend on well-founded empiric decisions in prescribing the pill for these patients. The basis for the decision should be a firm understanding of the pathophysiology and laboratory effects of OCs. This needs to be juxtaposed with an understanding of the efficacy and effects of the estrogen and progestational components of the birth control pill and their interactions with maintenance medications. Available evidence is reviewed for the following medical disorders: central nervous system disorders (depression, Wilson's disease, headaches, epilepsy, multiple sclerosis, and the eye); immunologic and connective tissue diseases; diseases of the endocrine system, the gastrointestinal system, the genitourinary system, the memopoietic system; and skin disorders. 7% of women on OCs have increased or newly reported depression. Whether these are primarily psychogenic or metabolically derived is yet to be definitively determined. Wilson's disease can be exacerbated by OCs because of increased plasma ceruloplasmin and increased absorption of copper from the gastrointestinal tract. Headaches can be either a vague or a specific symptom, such as migraines, but 1/3 of these patients will become worse on OCs. There is good evidence that the headaches are caused by falling estrogen levels. There is no good evidence that epilepsy, in general, becomes worse on OCs. OCs have relatively no effect on the longterm prognosis in multiple sclerosis. Increased corneal sensitivity has been observed with OC use, and this has usually presented an intolerance to the use of contact lenses. This is primarily the result of increased edema of the cornea and changing of its contour. By inference, OCs cause some basic universal changes in the immunologic system. OCs have been reported as a cause of a rare form of rheumatoid arthritis, but the Royal College reports a decrease in incidence of cell-mediated immunologic disease, specifically rheumatoid arthritis in its more familiar form. There is no evidence that OCs markedly influence thyroid disease, but they do markedly alter thyroid function testing. OCs do not produce a chronic addisonian state nor do they inhibit the ability of the adrenal-pituitary axis to respond to stress. OCs can be used in thyroid disease but with some caution in hypothyroid states. They should not be used in patients with Cushing's syndrome and are not recommended in patients with adenomas. In general, estrogen works as an irritant to the gastric mucosa, but there is no increase in peptic ulcer diseases associated with OC use, and the incidence of duodenal ulcer disease is decreased. The most striking liver disease seen with OCs is cholelithiasis. The incidence is increased 2-fold. OCs should not be prescribed for patients with chronic renal disease because of the vascular effects as well as the reported increased risk of urinary tract infection. The Royal College report has shown a decreased incidence of iron deficiency anemia in patients on OCs. Various skin changes have been reported in women using OCs. The most common of these is chloasma. In all the diseases studied thus far, the use of OCs has not precipitated a catastrophic change.
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PMID:The use of birth control pills in women with medical disorders. 702 14

Between 1981 and 1993, 14 patients with tumoral adrenal disease were diagnosed and treated in the Urology Services of both Hospitals. Nature of the adrenal disease was functional in 8 patients (two carcinomas and six pheochromocytomas) and non-functional in the rest (three carcinomas, two adenomas and one myelolipoma). Reference is made to the clinical manifestations and laboratory tests related to hormonal activity, depending on whether the tumour is functional or non-functional, chromaffin or non-chromaffin. Patients with functional carcinomas had Cushing's syndrome, with very clear virtilization signs. Urine 17-hydroxycorticosteroid, 17-cetosteroides and cortisol were all increased, same as plasma cortisol. Patients with pheochromocytomas had hypertension and headaches (six patients), sweating (five patients), anxiety (four patients) and loss of weight (two patients). All of them had increased urine vainillylmandelic acid and catecholamines. Clinical signs and symptoms of non-functional tumours were related to bulk growth and size (in the three carcinomas), and sometimes was highly anodyne, or even absent (in the two adenomas and the myelolipoma), the cause of discovery being accidental during an ultrasound examination. An analysis is made of the different imaging diagnostic procedures performed, such as IVU (performed in 13 patients) with a 38.4% resolutory power; ultrasound (performed in 11 patients) with an 81.8% resolution; CAT (performed in 6 patients) with a 100% resolution capacity and arteriography (performed in 3 patients) with a 100% resolution power, although patients had previously undergone ultrasound and CAT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical features, diagnosis, and treatment of tumor lesions arising in the adrenal gland]. 777 Dec 35

A 57-year-old woman was admitted to our hospital with occipital headache and nausea. She had severe hypertension (192/122mmHg), hypokalemia (2.8mEq/l) and fasting hyperglycemia (127 mg/dl). Further examination revealed elevated plasma ACTH (124pg/ml) and cortisol (26.5 mu g/dl) with a lack of diurnal rhythm. Plasma ACTH or cortisol did not increase by injection of corticotropin releasing hormone (CRH). Rapid ACTH test resulted in an exaggerated response of plasma cortisol. Abdominal MRI scan showed a left adrenal tumor. Since the bilateral adrenal venous blood sampling revealed a significant increase of cortisol on the left, left adrenalectomy was performed. Histological examination of the resected adrenal gland revealed marked cortical hyperplasia. Postoperative investigations revealed that despite a small dose of steroid replacement for only 20 days, plasma ACTH level was decreased for a period of 6 months. Both plasma ACTH and cortisol increased by a CRH injection 38 days after surgery. CRH test during bilateral inferior petrosal sinus sampling indicated that this patient had no functioning pituitary tumor. Although the exact mechanism of high plasma ACTH level in this case was unknown, these findings suggest that any substance secreted from primary adrenal nodular hyperplasia adrenal nodular hyperplasia may stimulate pituitary ACTH production. This is a very rare case of Cushing's syndrome due to unilateral primary adrenal nodular hyperplasia with elevated plasma ACTH.
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PMID:[A case of unilateral primary adrenal nodular hyperplasia with elevated plasma adrenocorticotropin (ACTH)]. 785 19

We retrospectively evaluated our experience with phaeochromocytoma from January 1986 to December 1995. There were 18 patients with surgically-proven phaeochromocytoma: three males, 15 females, aged 12-81 years (mean 42 years) at diagnosis. Sixteen were hypertensive; only 6/18 presented with two or more of the classical triad of headaches, palpitations and diaphoresis. One patient presented with hypertensive crisis. Duration of symptoms prior to diagnosis was 2 weeks to 6 years, mean 16.4 months. Sixteen patients had adrenal tumours and two had extra-adrenal tumours or paragangliomas. One had bilateral adrenal tumours and two had a combination of both adrenal and extra-adrenal tumours. There were four familial cases: two had multiple endocrine neoplasia type IIA (MEN-IIA), one had neurofibromatosis type I (NF-I) and one von Hippel-Lindau (VHL) disease. One patient had Cushing's syndrome arising from ectopic production of adrenocorticotropic hormone (ACTH) by the phaeochromocytoma. Disease was recurrent in three patients. Pre-operative diagnosis was confirmed mainly by elevated urine vanillylmandelic acid (VMA) and/or catecholamine levels. Twelve patients had plasma catecholamine determinations: noradrenaline was elevated in all, adrenaline in six and dopamine in two. Pre-operative localization was by CT scan or MR imaging in all patients. At follow-up of 1-10 years (median 4.8 years), 15 patients were cured surgically while two were asymptomatic despite recurrence of disease. One patient with recurrent paragangliomas died post-operatively.
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PMID:Phaeochromocytoma: a ten-year survey. 909 89

A patient with chronic daily headaches developed overt signs of Cushing syndrome during treatment with serial occipital nerve block injections. Investigation demonstrated an exogenous source of corticosteroids as the cause of the Cushing syndrome in this patient, thus, implicating the corticosteroid component of the occipital nerve blocks. To our knowledge, this is the first report of Cushing syndrome caused by occipital nerve blockade. Caution is warranted in employing even usual therapeutic doses of synthetic corticosteroids, particularly in long-acting or depot preparations.
Headache 2001 Oct
PMID:Cushing syndrome induced by serial occipital nerve blocks containing corticosteroids. 1170 80

The clinical, therapeutic, and laboratory aspects of pituitary tumors are outlined. Sometimes tumor symptoms like headaches and visual disturbances are not present, while endocrine symptoms depend on the type of trophic cells involved: acromegaly for growth hormone, Cushing syndrome for cortico-melanotrophic hormone, amenorrhea-galactorrhea for prolactin, and rarely, symptoms related to thyrotropin or gonadotropin. Recently prolactin-secreting adenomas have been differentiated from chromophobic adenomas in routine diagnosis. The endocrine symptoms may be masked by estrogen-progestagen pills until tumor symptoms develop, when surgery is mandatory. The results of surgery depend on the tumor volume. Selective adenectomy usually permits normal endocrine function afterward. These tumors may also be treated pharmacologically, e.g., with L-DOPA or dibromoergocryptine. The results of treatment are followed by pre- and postoperative radioimmunoassay of pituitary hormones.
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PMID:[Pituitary tumors]. 1225 17


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