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The course of pregnancy achieved after bromocriptine therapy is described in nine patients with radiologically evident prolactin-secreting pituitary tumors. In six patients no complications occurred. No changes in sellar size or secondary endocrine deficiencies developed. In three patients, however, complications developed between the 22nd and 24th weeks of pregnancy. Despite prior external pituitary irradiation, one patient developed transient bitemporal hemianopsia and one patient had apoplexy of the pituitary tumor with transient paresis of the left abducens nerve. A third patient developed parasellar expansion of the pituitary tumor with bone destruction and paresis of the right abducens and oculomotor nerves. After transsphenoidal surgery the paresis of both nerves disappeared. Microscopically, the tissue removed at surgery was a chromophobe adenoma with focal fibrosis and calcifications without recent hemorrhages. In the course of more than 100 pregnancies achieved in The Netherlands after bromocriptine therapy, five patients reportedly developed complications of the pituitary tumor. At present, patients in whom complications can be expected cannot be predicted by the size or configuration of the sella turicica or the magnitude of elevation of the plasma prolactin level. In two patients external pituitary irradiation did not prevent complications during pregnancy.
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PMID:The incidence of complications during pregnancy after treatment of hyperprolactinemia with bromocriptine in patients with radiologically evident pituitary tumors. 10 23

Chlorpromazine is frequently administered to patients with hyperprolactinemia to stimulate an increase in the serum levels of prolactin. A patient with a prolactin secreting adenoma is described in whom pituitary apoplexy developed in association with a hypotensive episode following the administration of 25 mg of chlorpromazine. Prolactin levels fell from more than 2,000 ng/ml to 340 ng/ml following infarction of the pituitary tumor. Pituitary apoplexy should be considered as a rare complication of chlorpromazine stimulation in a patient with a pituitary tumor.
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PMID:Pituitary apoplexy following chlorpromazine stimulation. 71 34

Pituitary Apoplexy is a rare but sometimes life threatening condition which requires prompt recognition and timely medical intervention to avoid catastrophic consequences. From January 1979 to June 1989 and total of one hundred and ninety eight pituitary tumor patients were operated on our hospital. Eighteen cases (9.1%) were diagnosed "pituitary apoplexy" according to histopathological findings. The group consisted of twelve men and six women ranging in age from twenty two to sixty one years with a mean of forty. There were three cases of prolactin-secreting adenomas (16.7%), four growth-hormone secreting adenomas (22.2%), and eleven nonfunctional adenomas (61.1%) with an incidence of 6.1%, 8.3%, and 11.4% respectively (P > 0.05). Clinical manifestation occurred acutely in 66.7% and nonacutely in 33.3%. The patients presented with headaches (100%), visual impairment (83.3%), visual field defects (66%), disturbed consciousness (22%), fever and meningismus (11%). Radiological examinations able to demonstrate abnormalities included plain skull films (84%), computed tomography (84.6%), and angiography (93.8%). Various investigations of endocrine function pre and post operatively showed a deficient gonad axis (53%, 62.5%), adrenal axis (26.7%, 56.2%), and thyroid axis (20%, 43.8%). Sixteen cases received a transsphenoid operation and three cases underwent a transfrontal craniotomy. No case of mortality was reported. Postoperative radiotherapy was given to nine cases and nine cases were followed up on a regular basis. Therefore, our retrospective study suggests that pituitary apoplexy is not uncommon and has an acute clinical presentation. No particular tumor type was prone to occur. Various radiological examinations could define perisellar abnormalities. With a decreasing order of hormone deficiency, gonad, adrenal and thyroid axis were observed during the course of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pituitary apoplexy: a study of eighteen cases]. 133 26

A case of intracranial arterial vasospasm caused by pituitary apoplexy after head trauma is reported. In this case, pituitary apoplexy was secondary to head trauma, and the vasospasm was thought to be due to subarachnoid hemorrhage from a pituitary tumor. No such case has previously been reported in the literature.
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PMID:Intracranial arterial vasospasm associated with pituitary apoplexy after head trauma--case report. 169 53

The authors report a case of a patient with a pituitary tumor, in which pituitary apoplexy occurred only in the suprasellar part of the tumor. A 26-year-old woman suffered from abrupt worsening of vision and headache. A CT scan showed a dumb-bell-shaped tumor extending to the suprasellar region, in which an irregularly shaped low density area suggesting a liquidized hematoma was seen. The rapid worsening of her symptoms was highly indicative of pituitary apoplexy. The first operation was performed through the transsphenoidal route. There was no evidence of intratumoral hematoma in the intrasellar tumor, which could be removed successfully. However, the suprasellar mass could not be reached because of the hardness of the diaphragma sellae and the presence of a normal pituitary gland. MRI and CT cisternography after this first operation showed a narrow opening of the diaphragma sellae. The second operation using right frontotemporal craniotomy disclosed a suprasellar mass, which consisted of an old hematoma and a necrotic tumor. The tumor was sub-totally removed. The patient's visual acuity improved after the second operation. Although transsphenoidal surgery is the treatment of choice in patients with pituitary apoplexy, the selection of the surgical route should be made only after careful neuroradiological evaluation with regard to the extrasellar extension of the tumor.
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PMID:[Pituitary apoplexy with localized hematoma in the suprasellar region]. 203 17

Hypopituitarism is a major manifestation of pituitary adenoma apoplexy. We postulated that the acute deterioration in pituitary function may be caused by compression of portal vessels and the pituitary stalk, secondary to a sudden increase in intrasellar contents. If this were the case, one would predict improvement in pituitary function to occur after surgical decompression. We studied pituitary function in eight patients presenting with the clinical syndrome of pituitary adenoma apoplexy before and on multiple occasions after urgent surgical decompression. Partial or complete hypopituitarism was seen in all subjects at the time of presentation. Serum cortisol levels were inappropriately low (5.9 +/- 1.4 micrograms/dL; 162.8 +/- 38 nmol/L) for the degree of stress in seven patients and appropriately elevated in only one subject (55.3 micrograms/dL; 1525.7 nmol/L). High normal increments in cortisol levels were noted in three subjects given test doses of cosyntropin. Patients were given glucocorticoids before, during, and for 2 days after surgery. Serum cortisol concentrations measured on or after the third day when glucocorticoids had already been stopped were normal in seven subjects and consistently low in one. These seven subjects were discharged on no replacement and were subsequently documented by dynamic testing to have normal pituitary-adrenal function. Gonadal function improved in two of four men and in one of two women who had hypogonadism on presentation. Improvement in thyroid function was documented in two of three subjects with preoperative hypothyroidism. Gradual improvement and almost complete resolution of the neuroophthalmological abnormalities occurred days to weeks after decompression. These observations demonstrate that urgent surgical decompression after pituitary tumor apoplexy was associated with improvement not only in neurological defects but also in pituitary function. The rapid improvement in pituitary function indicates not only that the hypopituitarism was reversible, but also that it might be caused by compression of the portal circulation and pituitary stalk by the sudden increase in intrasellar contents.
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PMID:Improvement of pituitary function after surgical decompression for pituitary tumor apoplexy. 216 68

Many neurologic disorders, such as eclampsia, pseudotumor cerebri, stroke, obstetric nerve palsies, subarachnoid hemorrhage, pituitary tumors, and choriocarcinoma, can develop in the pregnant patient. Maternal mortality from eclampsia, which ranges from 0 to 14%, can be due to intracerebral hemorrhage, pulmonary edema, disseminated intravascular coagulation, abruptio placentae, or failure of the liver or kidneys. Associated fetal mortality ranges from 10 to 28% and is directly related to decreased placental perfusion. Pseudotumor cerebri can be associated with serious visual complications; thus, the therapeutic goal is to prevent loss of vision. The risk of stroke in the pregnant patient is 13 times the risk in the nonpregnant patient of the same age. The major causes of stroke in pregnant patients are arterial occlusion and cerebral venous thrombosis. Lumbar disk prolapse is common in pregnant patients, and lumbosacral plexus injuries can occur during labor or delivery. In addition, peripheral nerve compression or entrapment syndromes are thought to be caused by the retention of fluid during pregnancy. The incidence of subarachnoid hemorrhage during pregnancy is 1 in every 10,000 patients, a rate 5 times higher than in nonpregnant women. Because of a proliferation of prolactin-secreting cells, the pituitary gland can enlarge dramatically during pregnancy, a change that can disclose a previously unknown tumor or cause a known pituitary tumor to become symptomatic. The incidence of choriocarcinoma is 1 in 50,000 full-term pregnancies but 1 in 30 molar pregnancies. This malignant tumor has a high rate of cerebral metastatic lesions. In addition to these disorders that develop during pregnancy, the pregnant state can affect numerous preexisting neurologic conditions, including epilepsy, headaches, multiple sclerosis, myasthenia gravis, spinal cord injury, and brain tumors. We discuss advice for patients with such conditions who wish to become pregnant, recommendations for medical and surgical management, and surgical considerations for neurologic complications during pregnancy.
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PMID:Selected neurologic complications of pregnancy. 225 22

Thirteen patients who presented with signs and symptoms of pituitary disease gave a history of classical pituitary apoplexy. Six presented with acute symptoms and in 7 the history antedated the admission by a mean of 887 days (range 365-2,190 days). All patients had an enlarged eroded sella. CT scans revealed a bleed in the tumor in 11 (histologically confirmed in all 8 patients operated), evidence of residual tumor in 1 and an empty sella (ES) in 1 patient. Hypopituitarism was present in 9, 4 were endocrinologically normal, 8 had visual problems requiring decompressive surgery and radiotherapy (RT) was given to 7 patients. They were subsequently followed for a median period of 730 days (range 365-3,385 days). During this time an empty sella developed in 5, 2 of whom had no surgery or RT; 4 remained endocrinologically normal, and a second hemorrhage occurred in 2 patients. Histological evidence of previous bleeds was noted in 6 of the 8 patients treated surgically. We conclude that apoplexy (1) may produce complete or partial tumor destruction with or without preservation of endocrine function; (2) recurrent, often silent, bleeding into a pituitary tumor appears to be a common event; (3) RT should be withheld unless recurrent tumor is documented (since at least 2 patients in this study have experienced spontaneous resolution of the tumor); and (4) the presence of an enlarged eroded fossa with an ES is reasonable presumptive evidence of an infarction of a pre-existing pituitary tumor.
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PMID:Classical pituitary apoplexy presentation and a follow-up of 13 patients. 274 25

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

A 34-year-old man with acromegaly was observed, and the clinical course and various endocrinological deficiencies occurring before, during and after the development of pituitary apoplexy were evaluated. Following the attack, the patient experienced acute reductions in growth hormone (GH) and other pituitary hormones, adrenohypophyseal insufficiency and transient diabetes insipidus which appeared subsequent to glucocorticoid therapy. The level of growth hormone in serum and cerebrospinal fluid (CSF) was measured synchronously, and the respective regressions of GH levels in serum and CSF were observed. The results demonstrated the utility of measuring hormonal levels in CSF in the clinical evaluation of pituitary apoplexy in a patient with a functioning pituitary tumor.
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PMID:Spontaneous remission of acromegaly after pituitary apoplexy following head trauma. 320 21


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