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

Among 135 consecutive cases of hypopituitary dwarfism, 42 related to detectable intracranial tumour or defect. In 13 cases the tumour had been previously operated and/or irradiated. In 29 others the defect was suggested by neurological abnormalities or headache, skull radiographs, ocular examination or by associated post-hypophyseal deficiency and was demonstrated by pneumoencephalography. When none of these associated abnormalities was found, pneumoencephalography failed to demonstrate any intracranial lesion. Among the 93 so-called idiopathic cases there was a large majority of males (60/93) with a history of birth difficulties (34/60) and especially of breech delivery (23/60). TSH, FSH/LH and ACTH deficiencies were associated to GH deficiency in 81% of patients with detectable intracranial lesions, 57% of male and 39% of female idiopathic cases. The number of patients with idiopathic isolated GH deficiency was similar in boys and girls, suggesting in them the hypothesis of a recessive autosomic genetic defect in spite of the scarcity of familial cases. Peculiar clinical associations may contribute to the diagnosis.
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PMID:[Etiology and associations of pituitary dwarfism. Study of a series of 135 cases]. 20 86

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

Emergencies in pituitary disease are not common. They can result from the failure of the pituitary gland to secrete one or more pituitary hormones, or from neuro-ophthalmological symptoms due to the mass effect of an expanding hypothalamic-pituitary tumour. Loss of hormone secretion, particularly ACTH and, to a lesser extent, TSH, can rapidly become life-threatening and requires urgent replacement therapy. Acute severe hypopituitarism should be vigorously treated as an emergency with a glucocorticoid preparation. Neuro-ophthalmological symptoms such as visual impairment, sudden onset of severe headache and alteration of the level of consciousness should prompt appropriate radiological investigations, since this may well call for emergency surgery.
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PMID:Pituitary gland emergencies. 173 97

Aneurysms of the sellar region are commonly mistaken for pituitary adenomas, since they have similar clinical, endocrinological and neurological symptoms. The authors describe three patients with giant aneurysms of the internal carotid artery which were initially diagnosed as pituitary tumors. In all patients the clinical presentation was nonspecific, and consisted mainly of neurological symptoms such as headaches and visual field defects. Endocrine abnormalities were also found in the three cases. Patient no. 1 had short stature, lack of GH response to clonidine stimulation, low IGF-1 levels and blunted TSH response to TRH. Patient no. 2 had gonadotropin deficiency and patient no. 3 had hyperprolactinemia. CT scans showed a densely enhanced lesion in all patients, which was heterogeneous in one case and homogeneous in the remaining. Carotid angiography confirmed the diagnosis of aneurysm. Preoperative angiographic studies are necessary for the differential diagnosis of an aneurysm from a pituitary tumor. Furthermore, these studies could prevent the serious consequences of a transsphenoidal surgical approach in misdiagnosed cases.
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PMID:Giant aneurysms of the sellar region simulating pituitary adenomas: a diagnosis to be considered. 180 16

Two cases of TSH-secreting pituitary adenoma were reported. Endocrinological and immunohistochemical features of these cases were described and problems in diagnosis and treatment of the rare disease are discussed. [case 1] A 28 year-old woman suffered from hyperthyroidism with a relatively high value of serum TSH (T3; 350 ng/dl, T4; 10.0 micrograms/dl, TSH; 24.5 microU/ml). She was treated with antithyroid drug and then underwent subtotal thyroidectomy. Although the levels of serum T3 and T4 were lowered to within normal range, the level of serum TSH still remained high. One month later, she developed frontal headache, amenorrhea and bitemporal hemianopsia. A CT scan showed an enhanced mass in the sellar and suprasellar region. Preoperative endocrinological studies showed elevated values of TSH (47 microU/ml) and its alpha-subunit (9.0 ng/ml). The levels of both T3 (190 ng/dl) and T4 (10.0 micrograms/dl) were near the upper normal limit. Serum TSH was suppressed by administration of exogenous T3, but did not respond to exogenous TRH, l-Dopa nor bromocriptine. Under the diagnosis of TSH-secreting pituitary adenoma, the patient was operated on by craniotomy and received local radiation therapy (50 Gy). In 1990, 12 years after the treatment, she is well and endocrinologically normal. Immunohistochemical study revealed that most tumor cells were positive for TSH. [case 2] A 28 year-old woman visited our hospital for examination of hyperthyroidism. Serum level of TSH was detectable (4.5 microU/ml). A CT scan performed at that time disclosed no pituitary tumor. Thyroid function was normalized by antithyroid drug, but the level of TSH was still high and progressively increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of TSH-secreting pituitary adenoma; endocrinological, diagnostic and therapeutic approach to the disease]. 194

Current views on cluster headache pathogenesis indicate a primary central nervous system dysfunction, in particular a hypothalamic involvement. To confirm the hypothalamic involvement in cluster headache we evaluated the hypothalamic-pituitary axis responsiveness with the thyrotrophin releasing hormone (TRH) test. A dose of 200 micrograms of TRH was administered i.v. to nine healthy controls, 32 patients with cluster headache during cluster period and 16 in remission period. Delta maximum thyrotrophin (TSH) was significantly lower in patients with cluster headache during cluster period (p less than 0.05 versus healthy controls and cluster headache patients in remission). No difference was observed between healthy controls and cluster headache patients in remission. A monoaminergic dysfunction at the hypothalamic level is hypothesized.
Cephalalgia 1990 Oct
PMID:Neuroendocrine dysfunction in cluster headache. 227 93

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

Primary hypothyroidism may be associated with enlargement of the sella turcica, due to thyrotroph hyperplasia, in its turn due to the lack of feedback control by thyroid hormones. It may develop independently of the severity or of the duration of thyroid failure. A 42-year-old woman was referred to us. She presented us with a CT scan compatible with a pituitary microadenoma, in the left part of the sella. The patient showed obvious signs of myxedema, due to subtotal thyroidectomy which had been performed 14 months before, because of the presence of multinodular goiter. After operation, the patient has been discontinuously and inappropriately treated with desiccated thyroid. She complained of headache, nausea, galactorrhea without amenorrhea. Serum T4 (0.8 micrograms/dl), serum T3 (47 ng/dl) and TSH (174.5 +/- 60.1 mU/l: M +/- SD of 4 assays) were compatible with primary hypothyroidism as confirmed by TSH hyper-response to i.v. TRH (200 micrograms) and i.v. domperidone (10 mg), and by the normal TSH decrease after orally administered 2.5 mg bromocriptine or 90 min continuously infused 800 micrograms GHIRH. Moreover, an abnormal GH response to TRH was observed, whereas basal and appropriately stimulated PRL levels were normal. Serum alpha-subunit was marginally high (5.92 ng/ml), but alpha-subunit/TSH molar ratio fell within the normal range (0.1 molar ratio). Complete suppression of basal and TRH stimulated TSH values was achieved after a 14-day L-T3 (120 micrograms per day) and 4-month L-T4 (200 micrograms per day) administration. L-T4 treatment, first administered at suppressive doses (200 micrograms per day for 4 months) and subsequently at substitutive doses (150 micrograms per day for 2 months), induced complete remission of symptoms along with normalization of the CT scan picture.
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PMID:Pituitary enlargement in post-surgical hypothyroidism misdiagnosed as thyrotroph neoplasia. Report of a case. 262 26

The diurnal rhythmicity of serum prolactin (PRL) and the PRL and thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) were studied in 31 cluster headache patients (4 chronic cases) and 14 healthy controls. Sixteen of the patients were studied both during clinical remission and headache periods. In males the nocturnal PRL peak was blunted during remissions as compared with that in cluster periods and that in control individuals. The 24-h mean PRL levels were lower during remission and cluster periods than in the controls. There were no significant differences in the PRL levels between female patients and controls. Headache attacks were often associated with increases of serum PRL levels. The PRL response to TRH was lower in the female patients but not in the male patients as compared with controls. The maximum testosterone levels were lower during cluster periods than during clinical remission but not when compared with controls. Serum levels of luteinizing hormone, follicle-stimulating hormone, progesterone, estradiol, T3, T4, and TSH did not differ between patients and controls. The results suggest an altered regulation of PRL secretion not only during active cluster periods but also during symptom-free intervals. The possible influence of sleep, estradiol, testosterone, medication, pain, and serotoninergic and dopaminergic mechanisms are discussed.
Cephalalgia 1987 Mar
PMID:Prolactin in cluster headache: diurnal secretion, response to thyrotropin-releasing hormone, and relation to sex steroids and gonadotropins. 310 37

Ten acromegalic patients were treated with the somatostatin analogue SMS 201-995 (SMS) for 3-38 weeks in various doses and by different administration routines (thrice daily or multiple sc injection). Plasma GH daily profiles, plasma IGF-I, urinary GH, serum TSH, IRI and fasting blood glucose (FBG) concentrations were measured before and during SMS treatment. Plasma GH rapidly decreased within one hour in all patients and was suppressed for at least 4 h after a 50 micrograms sc injection of SMS in 8 patients. Multiple injections of 300-600 micrograms/day SMS (25-50 micrograms X 12) suppressed GH throughout the day. Plasma IGF-I was completely normalized in 4 patients, and, in all but one of the others, decreased markedly. Urinary GH decreased within the first week of treatment in all patients and normalization was obtained in 3 patients. Shrinkage of the pituitary tumor, as determined by CT or MRI, was observed in 7 of 9 patients. Other clinical improvements, such as diminution or complete disappearance of swelling of soft tissues, excessive perspiration, and headache, were observed in 7 of 8 patients. Changes in serum TSH, IRI and FBG were seen in 3-4 patients, but without any apparent clinical problems. In conclusion, SMS is a useful clinical tool for treatment of acromegaly, and a multiple sc injection method seems to be preferable.
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PMID:Treatment of acromegaly with long acting somatostatin analogue SMS 201-995. 322 51


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