Pituitary Apoplexy due to Pituitary Adenoma Infarction

Cause of pituitary apoplexy has been known as hemorrhage, hemorrhagic infarction or infarction of pituitary adenoma or adjacent tissues of pituitary gland. However, pituitary apoplexy caused by pure infarction of pituitary adenoma has been rarely reported. Here, we present the two cases pituitary apoplexies caused by pituitary adenoma infarction that were confirmed by transsphenoidal approach (TSA) and pathologic reports. Pathologic report of first case revealed total tumor infarction of a nonfunctioning pituitary macroadenoma and second case partial tumor infarction of ACTH secreting pituitary macroadenoma. Patients with pituitary apoplexy which was caused by pituitary adenoma infarction unrelated to hemorrhage or hemorrhagic infarction showed good response to TSA treatment. Further study on the predisposing factors of pituitary apoplexy and the mechanism of infarction in pituitary adenoma is necessary.     

A case of subarachnoid hemorrhage with pituitary apoplexy caused by idiopathic hypertrophic pachymeningitis

Steroid therapy is considered to improve clinical symptoms in hypertrophic pachymeningitis. We present a 70-year-old man with idiopathic hypertrophic pachymeningitis, whose clinical signs progressively worsened despite steroid therapy. He died of subarachnoid hemorrhage (SAH) with pituitary apoplexy 2 months after the admission regardless of improvement of laboratory data and magnetic resonance imaging appearance by one-and-half-month steroid therapy. Autopsy revealed thickened dura mater supporting the diagnosis of hypertrophic pachymeningitis. Brain parenchyma is generally not affected by the disease; however, histological investigation suggested that inflammation of the dura caused damage to superior hypophyseal artery resulting in SAH and apoplexy in the anterior lobe of the pituitary gland. The higher dose and the longer duration of steroid therapy should have achieved in our case although most laboratory data recovered within the normal range. The aggressiveness of hypertrophic pachymeningitis must be evaluated by clinical signs rather than by laboratory data or imaging examinations.     

Coil embolization of ruptured frontopolar artery aneurysm: Case report

Distal anterior cerebral artery aneurysms are infrequent. The most common location is at the bifurcation of the pericallosal and callosomarginal arteries. Cerebral artery anomalies can sometimes, at least partially, explain aneurysm formation in less common locations in relation to hemodynamic stress caused on the vascular wall. We report a very rare case of subarachnoid hemorrhage due to a ruptured frontopolar artery aneurysm as a part of an anomalous anterior cerebral artery complex that was, for the first time, treated with endovascular coiling.     

A Large Ruptured Anterior Communicating Artery Aneurysm Presenting with Bitemporal Hemianopsia

Anterior communicating artery (ACoA) aneurysms sometimes present with visual symptoms when they rupture or directly compress the optic nerve. Giant or large ACoA aneurysms producing bitemporal hemianopsia are extremely rare. Here we present an unusual case of bitemporal hemianopsia caused by a large intracranial aneurysm of the ACoA. A 41-year-old woman was admitted to our neurosurgical department with a sudden-onset bursting headache and visual impairment. On admission, her vision was decreased to finger counting at 30 cm in the left eye and 50 cm in the right eye, and a severe bitemporal hemianopsia was demonstrated on visual field testing. A brain computed tomography scan revealed a subarachnoid hemorrhage at the basal cistern, and conventional cerebral catheter angiography of the left internal carotid artery demonstrated an 18×8 mm dumbbell-shaped aneurysm at the ACoA. Microscopic aneurysmal clipping was performed. An ACoA aneurysm can produce visual field defects by compressing the optic chiasm or nerves. We emphasize that it is important to diagnose an aneurysm through cerebrovascular study to prevent confusing it with pituitary apoplexy.     

New method for the experimental production of subarachnoid hemorrhage

A new method for an experimental subarachnoid hemorrhage in a cat is described. It attempts to simulate closely a bleeding from a ruptured aneurysm. An approach through the mouth and presphenoid sinus offers to the internal carotid, cerebral anterior, media and anterior communicating arteries. Needle puncture produces local stress to the artery characteristic for aneurysm rupture. The bleeding occurs to the subarachnoid in a closed skull, since the bone opening untouched by the preparation. The method has been compared with other procedures for experimental subarachnoidal hemorrhage. The method is applicable to experimental studies on pathophysiological, metabolic and, vascular changes, after subarachnoid hemorrhage.     

Coexistence of aneurysmal subarachnoid haemorrhage and pituitary apoplexy: Case report and review of the literature.

A case of aneurysmal subarachnoid haemorrhage with associated haemorrhagic infarction of a growth hormone secreting pituitary macroadenoma is presented. The subarachnoid haemorrhage was not identifiable on CT, but was apparent on MRI. Angiography revealed a 7mm right posterior communicating aneurysm, a 3mm left A1 segment anterior cerebral aneurysm, and vasospasm. Surgery was performed through a right pterional/subfrontal approach, clipping both aneurysms and debulking the tumour. The left A1 aneurysm was the site of subarachnoid haemorrhage. There was evidence of haemorrhagic infarction of the pituitary tumour. Although rupture of an aneurysm into a pituitary tumour has been previously reported, this is the first case reported of aneurysmal subarachnoid haemorrhage with coexisting pituitary apoplexy where the aneurysm had not bled directly into the pituitary tumour. The literature regarding the association between pituitary tumours and aneurysm is reviewed.     

Radiological Apoplexy and Its Correlation with Acute Clinical Presentation, Angiogenesis and Tumor Microvascular Density in Pituitary Adenomas

Objective

Pituitary apoplexy is life-threatening clinical syndrome caused by the rapid enlargement of a pituitary tumor due to hemorrhage and/or infarction. The pathogenesis of pituitary apoplexy is not completely understood. We analyzed the magnetic resonance imaging (MRI) of pituitary tumors and subsequently correlated the radiological findings with the clinical presentation. Additionally, immunohistochemistry was also performed to determine whether certain biomarkers are related to radiological apoplexy.

Methods

Thirty-four cases of pituitary adenoma were enrolled for retrospective analysis. In this study, the radiological apoplexy was defined as cases where hemorrhage, infarction or cysts were identified on MRI. Acute clinical presentation was defined as the presence of any of the following symptoms: severe sudden onset headache, decreased visual acuity and/or visual field deficit, and acute mental status changes. Angiogenesis was quantified by immunohistochemical expression of fetal liver kinase 1 (Flk-1), neuropilin (NRP) and vascular endothelial growth factor (VEGF) expression, while microvascular density (MVD) was assessed using Endoglin and CD31.

Results

Clinically, fourteen patients presented with acute symptoms and 20 for mild or none clinical symptoms. Radiologically, fifteen patients met the criteria for radiological apoplexy. Of the fifteen patients with radiologic apoplexy, 9 patients presented acute symptoms whereas of the 19 patient without radiologic apoplexy, 5 patients presented acute symptoms. Of the five biomarkers tracked, only VEGF was found to be positively correlated with both radiological and nonradiological apoplexy.

Conclusion

While pituitary apoplexy is currently defined in cases where clinical symptoms can be histologically confirmed, we contend that cases of radiologically identified pituitary hemorrhages that present with mild or no symptoms should be designated subacute or subclinical apoplexy. VEGF is believed to have a positive correlation with pituitary hemorrhage. Considering the high rate of symptomatic or asymptomatic pituitary tumor hemorrhage, additional studies are needed to detect predictors of the pituitary hemorrhage.     

Ruptured Anterior Spinal Artery Aneurysm: A Case Report

We present a case of a subarachnoid hemorrhage and vasospasm secondary to a ruptured anterior spinal artery aneurysm associated with a Chiari 1 malformation. To our knowledge this is the first reported spinal artery aneurysm with this association.     

Pituitary apoplexy in a child presenting with massive subarachnoid and intraventricular hemorrhage.

A case of pituitary apoplexy in a child with massive subarachnoid and intraventricular hemorrhage is reported. The patient presented with a sudden onset of headache, diminution of visual acuity and a bitemporal visual field defect. Computerized tomography revealed a massive subarachnoid hemorrhage with extension of blood into the third ventricle. Angiography did not show an aneurysm. The patient was operated on and altered blood within a necrotic pituitary adenoma was decompressed. His vision and field defect improved along with resolution of headache in the postoperative period.     

CTA指导破裂的前交通动脉动脉瘤显微夹闭术

目的 探讨CTA在破裂的前交通动脉瘤诊断和治疗中的作用.方法 对26例前交通动脉瘤破裂致自发性SAH患者进行术前CTA检查及CTA手术模拟,26例均行翼点入路开颅夹闭动脉瘤手术,以术前CTA与术中所见进行比较.结果 CTA对前交通动脉瘤的诊断与术中符合率100%,术前CTA与术中所见基本一致.结论 术前CTA检查和手术模拟对成功夹闭破裂的前交通动脉瘤具有较大的应用价值.     

Early operation of ruptured basilar artery aneurysm associated with bilateral carotid occlusion (moyamoya disease)

A 34-year-old Caucasian man presented with subarachnoid hemorrhage. Angiography revealed bilateral carotid occlusion at the cavernous sinus and an aneurysm at the basilar artery bifurcation. The whole brain was supplied with blood from the basilar artery and posterior cerebral arteries through a large number of collateral vessels to the internal carotid artery bifurcation, middle cerebral and anterior cerebral arteries: the moyamoya phenomenon. The aneurysm was clipped within hours of the subarachnoid hemorrhage. The relation between moyamoya disease and basilar artery aneurysms is discussed and some surgical and management considerations are given.     

Pituitary apoplexy associated with cabergoline therapy

Pituitary apoplexy is a rare medical emergency which results from hemorrhage or infarction in the pituitary gland. One of the predisposing factors is treatment with dopamine agonists, especially bromocriptine. We report a 20-year-old Chinese man with prolactinoma who developed pituitary apoplexy 6 weeks after initiation of cabergoline. He was treated conservatively with supportive therapy, and recovered well with no loss of pituitary function. A literature search was conducted and a review of the reported patients with pituitary apoplexy during treatment with dopamine agonists is discussed.     

Distal posterior cerebral artery aneurysm associated with multiple aneurysms

True congenital peripheral aneurysms of the cerebral arteries are rare and may constitute a special entity. We report a rare case of nonmycotic peripheral aneurysm of the posterior cerebral artery (PCA) found in association with aneurysms of distal middle cerebral artery (MCA), junction between basilar artery (BA) and superior cerebellar artery (SCA) and MCA trunk. Our present case was a 37-year-old man with a history of abrupt loss of consciousness. Cerebral angiography revealed a right PCA aneurysm originating at the junction between the trunk of the PCA and the posterior temporal branch, and also aneurysms of the right distal MCA, at the right BA–SCA junction and at the trunk of right MCA just distal to the anterior temporal artery. Distal PCA aneurysm causing subarachnoid hemorrhage was successfully clipped and all the other aneurysms were treated in a one-stage procedure. Pathological examination of the surgically excised distal PCA aneurysmal sac demonstrated no infectious etiology. There have not been any similar cases showing an association of vascular anomalies with distal PCA aneurysm. This is the only reported case with the association of nonmycotic peripheral aneurysms involving the MCA and PCA.     

Glue Embolization of Ruptured Anterior Thalamoperforating Artery Aneurysm in Patient with Both Internal Carotid Arteries Occlusion

Thalamoperforating artery aneurysms are rarely reported in the literature. We report an extremely rare case of ruptured distal anterior thalamoperforating artery aneurysm which was treated by endovascular obliteration in a patient with occlusion of both the internal carotid arteries (ICAs) : A 72-year-old woman presented with severe headache and loss of consciousness. Initial level of consciousness at the time of admission was drowsy and the Glasgow Coma Scale score was 14. Brain computed tomography (CT) scan was performed which revealed intracerebral hemorrhage in right basal ganglia, subarachnoid hemorrhage, and intraventricular hemorrhage. The location of the aneurysm was identified as within the globus pallidus on CT angiogram. Conventional cerebral angiogram demonstrated occlusion of both the ICAs just distal to the fetal type of posterior communicating artery and the aneurysm was arising from right anterior thalamoperforating artery (ATPA). A microcatheter was navigated into ATPA and the ATPA proximal to aneurysm was embolized with 20% glue. Post-procedural ICA angiogram demonstrated no contrast filling of the aneurysm sac. The patient was discharged without any neurologic deficit. Endovascular treatment of ATPA aneurysm is probably a more feasible and safe treatment modality than surgical clipping because of the deep seated location of aneurysm and the possibility of brain retraction injury during surgical operation.     

Saccular Aneurysm at the Anterior Communicating Artery Complex Associated with an Accessory Middle Cerebral Artery : Report of Two Cases and Review of the Literature

Accessory middle cerebral artery (MCA) is an infrequent vascular anomaly of the brain. Cerebral aneurysms associated with this anomalous artery are also very rare. To our knowledge, there have only been ten previous reports of an aneurysm associated with accessory MCA. The authors present two patients with accessory MCA-related aneurysms. A 38-year-old male and a 59-year-old female both presented with sudden-onset severe headache. In both patients, computed tomography (CT) scan revealed subarachnoid hemorrhage. A subsequent angiogram demonstrated an accessory MCA arising from the anterior cerebral artery (ACA) and a saccular aneurysm at the anterior communicating artery (ACoA) complex associated with an accessory MCA. Surgical clipping allowed for complete exclusion of the aneurysm from the arterial circulation. Based on our review of the ten cases of aneurysms associated with accessory MCA documented in the literature, we suggest that accessory MCA-related aneurysms can be classified according to whether the accessory MCA originates from the proximal A1 segment or from the ACoA complex. We also emphasize the importance of precise interpretation of preoperative angiograms and intraoperative precaution in determining the presence of this anomalous artery prior to temporary clip placement.     

Characteristics and Management of Residual or Slowly Recurred Intracranial Aneurysms

Objective

Residual aneurysm from incomplete clipping or slowly recurrent aneurysm is associated with high risk of subarachnoid hemorrhage. We describe complete treatment of the lesions by surgical clipping or endovascular treatment.

Methods

We analyzed 11 patients of residual or recurrent aneurysms who had undergone surgical clipping from 1998 to 2009. Among them, 5 cases were initially clipped at our hospital. The others were referred from other hospitals after clipping. The radiologic and medical records were retrospectively analyzed.

Results

All patients presented with subarachnoid hemorrhage at first time, and the most frequent location of the ruptured residual or recurrent aneurysm was in the anterior communicating artery to posterior-superior direction. Distal anterior cerebral artery, posterior communicating artery, and middle cerebral artery was followed. Repositioning of clipping in eleven cases, and one endovascular treatment were performed. No residual aneurysm was found in postoperative angiography, and no complication was noted in related to the operations.

Conclusion

These results indicate the importance of postoperative or follow up angiography and that reoperation of residual or slowly recurrent aneurysm should be tried if such lesions being found. Precise evaluation and appropriate planning including endovascular treatment should be performed for complete obliteration of the residual or recurrent aneurysm.     

A case of agenesis of the corpus callosum accompanied by a ruptured azygos anterior cerebral artery aneurysm and lipoma--a case report

A 53-year-old woman suffered from sudden onset of severe headache on February 28 in 1982. She was admitted to our hospital soon after onset. On admission, she had a severe headache and nausea, and her consciousness was drowsy. CT scan showed a marked subarachnoid hemorrhage with intracerebral and intraventricular hematoma, a separation of the lateral ventricles with enlargement of posterior horns, and deformity of anterior horn. By these findings, the patient was diagnosed as an agenesis of the corpus callosum with subarachnoid hemorrhage. Left carotid arteriogram revealed an azygos anterior cerebral artery and an aneurysm at the terminal portion of this artery. Surgery was performed on the 24 th day after subarachnoid hemorrhage. Operative finding revealed a little finger's head-sized tumor was situated over the right frontobasal artery. An azygos anterior cerebral artery aneurysm was clipped and tumor was removed. Pathological diagnosis of the tumor was a lipoma. Namely, she had an agenesis of the corpus callosum, an azygos anterior cerebral artery, an aneurysm and a lipoma. There are some reports in which an agenesis of the corpus callosum is accompanied with a lipoma and an azygos anterior cerebral artery is accompanied with an aneurysm. But a case of agenesis of the corpus callosum with an azygos anterior cerebral artery was rarely reported. So this rare case with these anomalies was reported and pathogenesis about the development of 4 anomalies was also discussed.     

垂体瘤卒中诊断和治疗的再探讨

目的探讨典型和不典型垂体瘤卒中的发病机制,从而为合理制定治疗方案和正确选择手术时机提供帮助。方法经临床表现和/或手术治疗及病理学诊断为垂体瘤卒中病例28例中,24例符合垂体瘤卒中的典型临床表现,另4例符合不典型垂体瘤卒中的诊断。分析垂体瘤卒中的临床表现、影像学表现、手术及病理发现与病程之间的关系及其在病程中各时期的影像学表现、手术发现及病理诊断的特征。结果根据典型垂体瘤卒中病程中不同阶段的临床症状体征、影像学、手术及病理特点,将病程分为早期梗死出血期和后期坏死期,手术全切率分别为87.5%(7/8)和100%(14/14)。不典型垂体瘤卒中的影像学、手术和病理均证实为瘤内陈旧性出血,手术全切率为75.0%(3/4)。结论典型垂体瘤卒中多因肿瘤梗塞后坏死并继发出血所致,急诊手术治疗目的是为了缓解症状。后期坏死期的手术效果明显优于早期梗死出血期,症状不显著者可采用激素替代保守治疗。不典型垂体瘤卒中以慢性瘤内出血为主要特征,无急诊手术治疗指征。     

Actively bleeding intracranial aneurysm demonstrated by CT angiography

CT angiography (CTA) is increasingly being utilized in the initial diagnosis of subarachnoid hemorrhage. While active bleeding from an intracranial aneurysm has been demonstrated on conventional angiography, CT angiogram findings of active aneurysmal hemorrhage are not well described. We present a case of an actively bleeding anterior communicating artery aneurysm demonstrated by CT angiography. The initial CTA demonstrated the extravasation of contrast from the anterior communicating artery. A second CT scan less than 1h later confirmed the ongoing hemorrhage, with extension of hemorrhage into the subarachnoid cisterns and the ventricular system. Recognition of active aneurismal hemorrhage by CTA may modify plan of treatment and follow-up imaging.     

Histopathological findings of the pituitary gland in cases of subarachnoid hemorrhage

Histopathological change of the pituitary gland in cases of the central nervous system disorder, especially in the cases of subarachnoid hemorrhage, was studied. Clinical materials were 23 cases who were died from subarachnoid hemorrhage due to aneurysmal rupture in the acute stage. Histopathological change was examined not only of the pituitary gland but also hypothalamus and the change due to increased intracranial pressure (midbrain hemorrhage and uncal herniation). Main histopathological findings of the pituitary gland are anterior pituitary necrosis and they are found in 8 cases out of 23 subarachnoid hemorrhage cases (34.9%). Histopathological changes in hypothalamus were hemorrhage or infarction, and these changes were present in 16 cases (70%). Eight cases with pituitary necrosis had shown hypothalamic lesions. Three cases out of 23 cases (17.4%) showed midbrain hemorrhage and uncal herniation and 3 cases out of these 4 cases had anterior pituitary necrosis. According to the angiographic findings, vasospasm tended to be severe and widespread in cases of anterior pituitary necrosis, meanwhile vasospasm did not tend to be severe or widespread in cases without anterior pituitary necrosis. It was suspected that the mechanism of the development of pituitary necrosis is related not only to the circulatory disturbance of the portal vessels due to mechanical compression on the pituitary stalk and acutely raised intracranial pressure at the moment of aneurysmal rupture, but also circulatory disturbance of the portal vessels due to vasospasm.