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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a 56-year-old man with sudden onset of retrobulbar headache and progressive loss of vision in his left eye is described. The anatomical position of the chiasm noted during surgical resection of a necrotic pituitary adenoma accounted for this patient's presentation of monocular blindness. We discuss the typical features of pituitary apoplexy and provide a pathophysiological explanation of these signs and symptoms. A differential diagnosis is given and appropriate treatment is described.
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PMID:Pituitary apoplexy presenting as monocular blindness. 261 Jul 64

The authors describe seven cases of pituitary adenoma with acute neurological symptoms (the so-called pituitary apoplexy), which were examined by magnetic resonance imaging (MRI). Four patients underwent surgery and the diagnosis of pituitary adenoma was histologically confirmed. In 3 patients, conservative treatment was decided and serial MRI examinations showed progressive decrease in size of the tumour, leading in one case to an empty sella. Computerized tomography (CT) was positive in all 7 cases, but less contributive than T1-weighted MRI images both for tumoral volume determination and detection of intratumoral haemorrhage. Although theoretical problems may arise concerning the diagnosis of acute intratumoral bleeding at an early stage, the authors emphasize the value of MRI in showing the extension of the tumor into the retroclival cistern and the cavernous sinus, especially when surgery is not performed in the acute period.
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PMID:MRI in the diagnosis of so-called pituitary apoplexy: seven cases. 269 19

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

Hemorrhage in a pituitary adenoma is a rare occurrence. Before computed tomography became the primary imaging modality for the sella, hemorrhage in pituitary adenoma was always diagnosed during operations or at autopsy. A patient with subacute hemorrhage in a nonfunctioning chromophobe pituitary adenoma with computed tomography findings is reported. The clinical presentation was unlike a pituitary apoplexy.
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PMID:Computed tomography of hemorrhage in a pituitary adenoma without apoplexy. 316 36

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

Twelve patients who developed mania after a brain lesion are reported. Ages ranged from 20 to 83 years. Five patients had brain tumors (three frontal meningiomas, one temporal meningioma, and one temporal astrocytoma), four patients had stroke lesions (one frontal, one temporal, and two thalamocapsular), two patients had a traumatic frontal closed head injury, and one patient had a pituitary adenoma resection. Although seven patients had lesions restricted to the right hemisphere, four had bilateral or midline damage and one had a left hemisphere lesion. Damage to structures functionally connected to the obitofrontal cortex, mainly in the right hemisphere, seems to be associated with secondary mania. The possible roles of monoaminergic, genetic, and perinatal factors in the pathogenesis of secondary mania are discussed.
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PMID:Mechanisms of mania after brain injury. 12 case reports and review of the literature. 327 15

Twenty-three untreated patients with acromegaly for 6-46 yr who were followed for 2-13 yr were studied. High resolution computed tomographic scans in 11 patients revealed herniation of the subarachnoidal space into the pituitary fossa (empty sella) and an intrasellar cyst in 2. Suprasellar tumor extension developed during the follow-up period in only 1 patient. Eleven patients previously (in 10 patients more than 4 yr earlier) had been treated with bromocriptine; 6 of these patients at follow-up had a solid intrasellar adenoma. Six of the patients with an empty sella or intrasellar cyst had had symptoms suggesting pituitary apoplexy. The sellar volume did not increase during follow-up in any patient with an empty sella. Plasma GH levels (basal and mean concentrations during an oral glucose load) increased (greater than 50 ng/ml) in 3 and decreased in 3 patients during follow-up. Normalization of plasma GH levels was rare, and physical well-being with complete absence of acromegalic symptoms was reported by only 4 patients. These results demonstrate that GH-secreting pituitary tumors may remain stationary for extended periods of time and that complete or partial disappearance occurs frequently, probably as a result of pituitary adenoma infarction.
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PMID:The spontaneous course of pituitary adenomas and occurrence of an empty sella in untreated acromegaly. 372 23

Ten consecutive patients with subarachnoid hemorrhage (SAH) of unknown cause were examined for sellar abnormalities and pituitary dysfunction. The diagnosis of SAH rested on a typical history and the demonstration of blood in the cerebrospinal fluid (computed tomography (CT), lumbar puncture). Initial CT and four-vessel angiography were performed in all patients, and five had repeat angiography. Endocrinological assessment was done after the initial angiography, and abnormal findings from this first study were reassessed 3 months later. The follow-up study included a high resolution CT scan of the sellar region. One patient had panhypopituitarism. Insufficient growth hormone secretion alone or combined with a low plasma concentration of estradiol or testosterone was found in another seven patients. The sella was ballooned or enlarged in three patients, and four patients had at follow-up a partly empty sella. A spontaneous development of a partly empty sella from an adenoma with suprasellar extension was observed in the patient with panhypopituitarism. This patient had experienced pituitary apoplexy with resulting SAH. Based on sellar enlargement, an empty sella, and pituitary dysfunction, this pathogenesis was suggested in another three patients. Our findings suggest that hemorrhagic necrosis in a pituitary adenoma may be an important cause of SAH with normal angiography.
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PMID:Subarachnoid hemorrhage with normal cerebral angiography: a prospective study on sellar abnormalities and pituitary function. 380 31

The association of pituitary adenoma and adjacent cerebral aneurysm is not uncommon and acute hemorrhage into a pituitary adenoma is also a well recognized condition. However, the simultaneous occurrence of pituitary apoplexy with intracranial aneurysm is very rare. Such a case demonstrates the diagnostic difficulty in distinguishing between pituitary apoplexy and rupture of an aneurysm. We reported a patient with subarachnoid hemorrhage in whom a hemorrhage into the pituitary adenoma and a carotid-ophthalmic aneurysm was proven, and discussed the differential diagnosis and treatment. A 41-year-old man, who developed sudden severe headache with nausea and vomiting, was admitted to our hospital. Examination disclosed a mildly stuporous man with bilateral defects of upper lateral visual fields and lumbar puncture revealed subarachnoid hemorrhage. Plain radiographs of the skull showed an enlarged and eroded sella turcica. Carotid angiography revealed a left carotid-ophthalmic aneurysm. A plain CT scan demonstrated an acute suprasellar hematoma. A transsphenoidal operation was performed and postoperative course was uneventful.
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PMID:[Pituitary apoplexy with an unruptured carotid-ophthalmic aneurysm]. 401 Aug 80

The authors report a case of pituitary apoplexy that developed in a patient shortly after bromocriptine therapy was started for a growth hormone-secreting pituitary adenoma. The tumor was associated with visual impairment and ocular palsies, and was treated by transsphenoidal decompression. Although spontaneous tumor necrosis cannot be excluded, a causal role of bromocriptine treatment is suggested.
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PMID:Pituitary apoplexy in an acromegalic patient during bromocriptine therapy. Case report. 402 Apr 51


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