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

Sixty of 146 patients with intracranial neoplasms or arterial aneurysms had roentgenographic abnormalities of the sella turcica. These abnormalities were most commonly due to chromophobe adenoma, craniopharygioma, and acromegaly, but ten of them were caused by lesions arising distant to the sella. There were also three cases of empty sella syndrome. Headache, visual disturbance, and sexual dysfunction were the most frequent presenting complaints, with visual field abnormality being most common. Pituitary dysfunction was manifested most frequently by alterations in growth hormone level and gonadotrophin secretion and less frequently by hypothyroidism and adrenocortical insufficiency. When the abnormal sella was associated with evidence of symptomatic intracranial disease, endocrine dysfunction, or visual field compromise as evidence of an anatomically aggressive intracranial neoplasm, specialized neuroroentgenographic localizing procedures were usually positive, and treatment for most of the causative lesions was highly effective.
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PMID:Abnormal sella turcica. A tumor board review of the clinical significance. 29 8

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 authors employed a gonadotropin-releasing hormone agonist (GnRH-a) (D-His6-pro9-NET-GnRH) to treat 19 patients with symptomatic uterine leiomyomata, by daily subcutaneous injections (4 micrograms/kg) for 6 months. After therapy, patients were followed for 6 months without any therapy. Uterine volumes were measured by serial pelvic examinations and pelvic sonography. Measurements of serum estradiol, luteinizing hormone, and follicle-stimulating hormone were used to assess treatment response. Pituitary desensitization and hypoestrogenemia were achieved in all within 8 weeks, and in 18 of 19, hypoestrogenemia was maintained for the duration. Uterine volume at the conclusion of therapy (207.5 +/- 152.7 ml) was significantly reduced in all patients when compared with pretreatment sizes (420.8 +/- 276.4, P less than 0.05). Side effects included hot flashes (78%), vaginal dryness (32%), and transient frontal headaches (55%). All patients reported partial or complete relief from their symptomatic leiomyomata. Uterine volume at the conclusion of follow-up (345.4 +/- 195.7 ml) was greater than at the conclusion of therapy. Menses resumed in all patients within 4 to 8 weeks. In conclusion, GnRH-a therapy does not provide definitive therapy for symptomatic uterine leiomyomata but is effective in reducing the size of leiomyomata as a temporary measure. Gonadotropin-releasing hormone agonist therapy may be useful as an adjunct before myomectomy or hysterectomy and deserves further investigation.
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PMID:Efficacy of a gonadotropin-releasing hormone agonist in the treatment of uterine leiomyomata: long-term follow-up. 249 32

Pituitary adenomas encompass the endocrine, symptomatic or functionally active and the non-functional, null cell or functionally inactive. According to their sizes, they can be very small, also called microadenomas, or they can be very large, "invasive", or macroadenomas usually without clinical evidence of hypersecretion. The "invasive" pituitary adenomas usually grow beyond the confines of the sella turcica. These adenomas are characterized anatomically by displacement, distortion and compression of the adjacent sellar structures. They may destroy bone and penetrate into the nasal cavity or into the cavernous sinuses. They may distend the diaphragm sella and compress the hypothalamus and the optic chiasm and optic tracts or they may distort the cerebral cortex or penetrate into the third ventricle. "Invasive" pituitary adenomas are characterized clinically by visual disturbances, headaches, seizures, diabetes insipidus and by hypothalamic dysfunction mimicking some endocrinologically active pituitary adenomas. The diagnosis of invasive pituitary adenomas can be suspected clinically and can be confirmed by radiological evidence of destruction of the sella turcica and its boundaries or by neurosurgical intervention and finally by necropsy findings of "invasion" of the parasellar and suprasellar structures.
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PMID:The pathology of non-functional pituitary adenomas. 307 May 9

Intrasellar infection is characterized by pituitary dysfunction and damage to surrounding structures. In most cases patients have fever, headache, and visual disturbance and exhibit roentgenographic evidence of a mass. Suppurative infections may originate in the paranasal sinuses, meninges, or more distant foci and are commonest in the setting of preexisting pituitary adenomata. Pituitary tuberculosis may arise from hematogenous spread or extension of local lesions and may be confused with a variety of other granulomatous diseases. Congenital and acquired syphilis of the pituitary are more often diagnosed at autopsy or by the concurrence of pituitary dysfunction and serologic evidence of syphilis. Although viral infection may be associated with pituitary or hypothalamic dysfunction, overt hypophyseal infection is rarely documented. In contrast, a variety of parasites and fungi have been found in pituitary tissue. The diagnosis of pituitary infection should be considered when signs of intrasellar mass or pituitary dysfunction are accompanied by fever and other evidence of infection.
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PMID:Infectious disease in the sella turcica. 353 14

A 33-year-old male was admitted to the Department of Neurosurgery, Fukui Medical School with a complaint of headache. There were no neurological deficits on admission. Craniogram demonstrated a so-called "phantom sella". A computed tomography revealed a high density mass lesion and the mass was enhanced well, that mainly extended from the sella to the left middle cranial fossa. The left carotid angiogram revealed an avascular mass lesion extending from the sella to the left middle cranial fossa. Pituitary function tests revealed an extremely high serum prolactin (PRL) levels (70, 100 ng/ml). PRL response to TRH was delayed in peak and the high level continued. Serum PRL levels elevated to 90, 800 ng/ml at 180 min after injection of TRH. A biphasic response was demonstrated in response to CB-154 suppression test to PRL secretion, that is, CB-154 stimulated PRL release initially (up to 90 min) and suppressed thereafter. Serum PRL levels (178, 400 ng/ml) reached to peak about 90 min after CB-154 administration. Response of growth hormone (GH) and adrenocorticotropic hormone (ACTH) to insulin were also impaired. Craniotomy was performed. The tumor was partially removed and was diagnosed as a prolactinoma histologically. Tumor tissue removed was subjected to the monolayer culture and electron microscopic study. Their observations demonstrated hyperactive PRL secretion of the individual cells. A total dose of 5,000 rads was irradiated postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of male prolactinoma presenting extremely high serum prolactin levels and biphasic response to CB-154 suppression test]. 404 Dec 91

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

Anterior pituitary tumors account for nearly 18% of all intracranial tumors. Pituitary adenomas that cause hypersecretion of growth hormone lead to acromegaly in adults. Patients with acromegaly may present unique problems for the anesthetist because of the overgrowth of airway soft tissues; a difficult mask ventilation and challenging intubation can be expected. A careful preoperative assessment of the patient's airway is essential, and an awake oral or fiberoptic bronchoscopy may be necessary. Postoperatively, these patients are at risk for developing airway problems and diabetes insipidus; therefore, they warrant careful observation. A 42-year-old, 75-kg, ASA physical status III, white male presented 8 months after suffering a head injury in which he was knocked unconscious for approximately 3 minutes. He began experiencing severe headaches, visual changes, and a marked increase in the size of his hands and feet. Four months before admission, he underwent bilateral carpal tunnel repairs. The patient was diagnosed with acromegaly after an extensive endocrine and neurosurgical evaluation. This is a case report of a patient with acromegaly who underwent an elective transsphenoidal hypophysectomy.
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PMID:Acromegaly and transsphenoidal hypophysectomy: a case report. 808 20

81 patients with expansive lesion in the optic chiasm region were reviewed. Pituitary adenomas were diagnosed in 37 patients: 5 with acromegaly, 2 with prolactinoma and the remaining 30 with hormone inactive adenomas. Meningiomas were diagnosed in 39, craniopharyngiomas in 4 patients and chordoma in one patient. The most common symptom was visual disturbance in 86%, but headache, hormonal disturbance occurred as well. All patients with adenomas were endocrinologically evaluated after detailed ophthalmologic and neurologic examinations. 28 patients were transcranially operated, 5 transsfenoidally and transcranially and 4 only transfenoidally. After endocrinologic reevaluation all patients with adenomas had undergone postoperative radiotherapy. Tumor recurrence was diagnosed in 14 patients, while 6 patients underwent reoperation. The approach to surgical regimen depended on the size and localization of meningioma. Unilateral subfrontal approach was most frequent (35). Subtotal tumor ablation was performed in 5 (13%) patients. Craniopharyngiomas were diagnosed in 4 patients (2 adults and 2 children). Total tumor ablation was performed only in one case.
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PMID:[Expansive processes in the optic chiasm region]. 892 47

Pituitary stimulation tests are widely used to explore hypophyseal adenomas. There are few disadvantages, although a few cases of pituitary necrosis have been published. We report a new case with a dramatic outcome. A 30-year-old man with clinical signs of acromegalia and major visual disorders was found to have a voluminous macro-adenoma of the pituitary gland. Thirty minutes after beginning the stimulation test, the patient complained of major headache and experienced persistant vomiting for several hours. Brain magnetic resonance imaging the next day did not reveal evidence of pituitary necrosis. Sudden onset coma occurred one hour later. The CT scan demonstrated hemorrhagic necrosis of the adenoma. The patient died despite emergency surgery. Due to the risk of hemorrhagic necrosis of a pituitary adenoma, baseline assays may be sufficient for diagnosis in patients with clinical signs highly suggestive of pituitary oversecretion, especially when a voluminous tumor is involved. Rigorous clinical surveillance is required after stimulation tests.
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PMID:[Fatal hemorrhagic necrosis of pituitary macro-adenoma after a stimulation test]. 895 74


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