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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pituitary function was studied in nine patients who had recovered from pituitary apoplexy. All the patients recovered spontaneously; none required immediate surgery. Four of the patients had acromegaly, two had pituitary-dependent Cushing's syndrome, and a "functionless" pituitary adenoma was found in three. Low serum growth hormone concentrations were observed in three patients with acromegaly whereas the concentration remained increased in the fourth one. Of the two patients with Cushing's syndrome, a selective ACTH-deficiency developed in one and Nelson's syndrome appeared with excessive secretion of ACTH in the other. Transient or persistent hypofunction of the anterior pituitary occurred in al patients. Three patients underwent hypophysectomy after respective intervals of three, eight and 12 months after pituitary apoplex. The operation revealed a hemorrhage in one functionless adenoma and a large cyst in another one. In the third patient who had acromegaly, no signs of the pituitary apoplexy were observed at operation.
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PMID:Pituitary function after pituitary apoplexy. 70 35

A case of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, in which a pituitary growth hormone (GH) secretion deficiency of hypothalamic origin was revealed through neuro-endocrinological examinations, was described. The case was a 10-year-old girl, who had been suffering from generalized tonic seizures since age 5, four episodes of alternating hemiplegia since age 6, stunted growth since age 7, and simple partial motor seizures as well as gelastic seizures since age 8. Marked elevation of lactate and pyruvate in both serum and CSF, abundant ragged red fibers in biopsied muscle, and low density areas in the left occipital lobe and bilateral globus pallidus in addition to diffuse brain atrophy on CT scan and MRI of the head were demonstrated, although the activities of muscle enzymes complex I-IV were within normal ranges. Pituitary GH secretion was deficient under the loadings with insulin, L-DOPA, sleep, and a single growth hormone releasing factor (GRF) administration, but normal GH response was registered under the repetitive stimulation with GRF. Activities of other hormonal axes were normal. It is likely that short stature commonly observed in MELAS patients is due to hypothalamic dysfunction, which might be brought out by chronic ischemia and energy deficiency of the diencephalon based upon mitochondrial abnormality of that region. It is likely that gelastic seizure in this case is due to hypothalamic dysfunction.
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PMID:[Hypothalamic GH Deficiency and gelastic seizures in a 10-year-old girl with MELAS]. 187 57

A case of Eaton-Lambert syndrome associated with pituitary apoplexy is presented. It is thought to be the first reported case. The clinical features, electrophysiological findings and effects and side effects of therapeutic drugs are noted. Endocrinological dysfunctions are discussed in relation to pituitary disorder.
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PMID:Eaton-lambert syndrome associated with pituitary apoplexy--a case report. 255 61

Three patients with neurological injuries consistent with cerebral stroke subsequently developed pain over portions of the body contralateral to the injured hemisphere. Stereotaxic chemical hypophysectomy was used in the management of this pain after other surgical procedures and medical management had failed to provide relief. Postoperatively, all patients were treated for hypopituitarism. All developed transient diabetes insipidus, and one patient developed transient right third nerve palsy. No other complications were encountered. All three patients experienced significant pain relief within 48 hours of the procedure. By the date of discharge, two of the three patients reported complete, and the third greater than 80% pain relief. At the initial follow-up visit all patients were essentially pain-free. These patients have now been followed for 58, 39 and 19 months, and remain free of their original pain. During this time the intravenous administration of naloxone has failed to reproduce the preoperative pain. Pituitary function testing 1 year or more following operation demonstrated that none of the patients had an endocrinologically complete hypophysectomy. Recovery from transient diabetes insipidus was not associated with return of the original pain. The mechanism of action of stereotaxic chemical hypophysectomy in the relief of pain related to thalamic lesions remains unknown. The observation that naloxone failed to reproduce the preoperative pain casts doubt on the theory that augmentation of endogenous opiate release is the primary mechanism. Additional observations suggest that pain relief after hypophysectomy may be more directly the result of stimulation of a hypothalamic pain-suppressing mechanism than due to the elimination of pituitary hormones.
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PMID:The use of stereotaxic chemical hypophysectomy in the treatment of thalamic pain syndrome. 635 4

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

Pituitary adenomas presenting de novo with apoplectic symptoms are uncommon. Several series on pituitary adenomas with apoplexy have been reported but have emphasized clinical aspects, incidence, or radiographic appearance by computed tomography (CT) scan. We reviewed our 13 years' experience, focusing on pathological appearance. We identified 15 patients with pituitary adenomas whose first presentation to our institution was with apoplexy. By combining histological and intraoperative findings with more sensitive magnetic resonance imaging (MRI) scans, we were able to attribute 5 of 15 cases to bland infarction, five cases to hemorrhagic infarction, four cases to pure clot, and one to a remote hemorrhagic infarction leaving extensive residual fibrosis and hemosiderin. Despite extensive tumor necrosis, reticulin staining still allowed identification of specimens as adenomas. Immunohistochemical staining was informative in 13 of 15 cases and endocrine-inactive, weak gonadotroph and null cell adenomas predominated. Cases with the greatest interval between symptom onset and surgery showed peripheral rim enhancement by MRI. Pathologically, this corresponded to granulation tissue, T cell lymphocytic infiltration, and atrophic pituicytes at the edge of the infarction or hemorrhage. Occasionally this reaction overshadowed the necrotic adenoma and contributed to diagnostic confusion. Our finding of lymphocytic inflammation in pituitary adenomas that have undergone an apoplectic event may suggest at least a modest immune-mediated response to damaged anterior pituitary tissue.
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PMID:Pathological correlates of pituitary adenomas presenting with apoplexy. 982 4

We describe a 72-year-old woman with a history of acute myeloid leukemia who developed pituitary apoplexy associated with thrombocytopenia secondary to chemotherapy. She presented with new onset severe headache, nausea, vomiting and blurred vision. Initial physical examination was unremarkable. CT scan of the head was initially negative. Upon admission for further work up, She developed a high-grade fever, hypotension and obtundation. Subsequent physical examination revealed bitemporal visual fields defects and decreased visual acuity. Repeat imaging of head revealed a hemorrhagic pituitary mass compressing the optic chiasm. Laboratory results were compatible with the diagnosis of pan-hypopituitary syndrome. She received high dose steroids and was transferred for transnasal sphenoidotomy decompression surgery. The visual defects improved postoperatively. A literature review of Pituitary apoplexy is presented. Pituitary apoplexy secondary to thrombocytopenia has never been reported.
Pituitary 2000 Oct
PMID:Pituitary apoplexy in a patient with acute myeloid leukemia and thrombocytopenia. 1114 94

Pituitary macroadenomas are rare in children and adolescents, and when encountered are usually hormone secreting. Symptomatic pituitary non-secreting macroadenoma apoplexy in an adolescent is rare and potentially life-threatening. A 15 year-old patient is described, hospitalized due to headache, fever and photophobia 4 days prior to admission. A meningeal syndrome was postulated, based on clinical examination and cerebrospinal fluid testing. However, clinical examination and hormone testing revealed partial failure of the anterior pituitary. Computed tomography of the brain demonstrated a space-occupying lesion of the pituitary. Magnetic nuclear resonance imaging suggested the presence of a pituitary macroadenoma. Hypophysectomy was performed. Histological examination revealed an extensive infarction of a pituitary adenoma. Hormonal substitution with thyroxine and corticosteroids was administered. This report emphasizes that pituitary non-secreting macroadenoma apoplexy may rarely be the cause of headache and fever in an adolescent, thus causing difficulties in differential diagnosis from acute meningitis.
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PMID:Pituitary non-secreting macroadenoma apoplexy in an adolescent. patient report and review of the literature. 1250 64

A case of sudden, unexpected death due to hemorrhage into a large, previously undiagnosed pituitary adenoma (pituitary apoplexy) in a 41-year-old man is presented. Pituitary adenomas are frequent intracranial tumors with usually benign prognosis. Acute hemorrhage into the tumor is a severe and potentially fatal complication, if not diagnosed and treated early, and occurs in up to 10% of cases. Sudden tumor enlargement due to the hemorrhage with compression of vessels and neural tissue at the skull base may result in coma and death without preceding symptoms leading to forensic investigations as demonstrated by this case report.
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PMID:Sudden death due to pituitary apoplexy. 1293 25

A thirty-eight year-old lady with a history of bilateral adrenalectomy for Cushing's disease seven years previously, presented with sudden onset of severe headache, nausea, vomiting and loss of consciousness. She was somnolent and confused. She had neck stiffness, sixth nerve palsy and mydriasis on the left side. Computerized tomography (CT) and magnetic resonance imaging (MRI) studies revealed a non-homogeneous, grade IV D pituitary mass lesion associated with hemorrhage in the chiasmatic, interhemispheric, cerebellopontine, perimesencephalic cisterns and a hematoma within the frontal lobe. Angiography showed only bilateral elevation of horizontal segments of the anterior cerebral arteries. According to this angiographic evidence, it was presumed that the subarachnoid hemorrhage and the intracerebral hematoma were linked to pituitary adenoma apoplexy. ACTH level was 450 pg/ml. The hemorrhagic lesion with suprasellar extension was totally removed by left pterional craniotomy. Histological examination revealed a necrotic, ACTH-secreting pituitary adenoma. Even though apoplexy is a well known complication of pituitary adenomas, to our knowledge subarachnoid hemorrhage and intracerebral hematoma as a result of pituitary apoplexy in the context of Nelson's syndrome has not previously been reported.
Pituitary 2002
PMID:An unusual presentation of Nelson's syndrome with apoplexy and subarachnoid hemorrhage. 1455 76


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