ABSTRACT
We report a case of bilateral vertebral artery (VA) dissecting aneurysm presenting subarachnoid hemorrhage (SAH). It was difficult to decide which side was responsible for SAH because the patient's symptom and head CT suggested that the left VA aneurysm had ruptured, but angiography and MRA showed an irregular pearl and string sign on the right side. He was successfully treated by trapping of the right VA dissecting aneurysm and we confirmed by intraoperative evaluation that the right VA dissecting aneurysm had ruptured. The left unruptured aneurysm decreased its size spontaneously. In the treatment of the bilateral VA dissecting aneurysms, angiography needs to be performed over and over again because contralateral unruptured aneurysm may grow or rupture due to increased hemodynamic stress. Various combinations of direct sugery with or without arterial reconstruction and endovascular treatment should be considered when treating bilateral VA dissecting aneurysms.
Subject(s)
Aneurysm, Ruptured/complications , Aortic Dissection/complications , Subarachnoid Hemorrhage/etiology , Vertebral Artery , Aortic Dissection/diagnosis , Aortic Dissection/surgery , Aneurysm, Ruptured/diagnosis , Aneurysm, Ruptured/surgery , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Tomography, X-Ray Computed , Vascular Surgical Procedures , Vertebral Artery/diagnostic imaging , Vertebral Artery/surgeryABSTRACT
A 51-year-old male presented with laceration of the bilateral intracranial internal carotid arteries (ICAs) manifesting as acute subdural hematoma (SDH) after a fall of 3 m. Brain computed tomography showed acute SDH appearing as irregular mixed high and low density and causing midline shift. During the operation, massive liquiform hematoma flowed out from the deep portion around the cranial base and systemic blood pressure decreased abruptly. Hemostasis was impossible and he died soon after the operation. Autopsy revealed skull fractures in the bilateral sphenoidal, orbital, temporal, frontal, parietal, and occipital bones, and laceration of the bilateral ICAs in the cavernous sinuses at the fracture sites. Acute SDH can be caused by laceration of the ICA.
Subject(s)
Carotid Artery Injuries/diagnostic imaging , Carotid Artery Injuries/etiology , Carotid Artery, Internal/diagnostic imaging , Fractures, Closed/complications , Fractures, Closed/diagnostic imaging , Hematoma, Subdural, Acute/diagnostic imaging , Hematoma, Subdural, Acute/etiology , Skull Base/injuries , Accidental Falls , Carotid Artery Injuries/pathology , Carotid Artery, Internal/pathology , Fatal Outcome , Fractures, Closed/pathology , Hematoma, Subdural, Acute/pathology , Humans , Male , Middle Aged , Radiography , Skull Base/diagnostic imaging , Skull Base/pathologyABSTRACT
OBJECT: The origin of multinucleated giant cells in glioma has not been made clear. In a previous paper the authors studied multinucleated giant tumor cells by using mitosis-specific phosphorylated antibodies to determine the phosphorylation of intermediate filaments and demonstrated that these cells stay in the early mitotic stage, undergoing neither fusion nor degeneration. In the current study the authors investigated the possible genetic causes of multinucleated giant tumor cells. METHODS: Cultured mono- or multinucleated human glioma cells were immunostained with monoclonal antibodies (mAbs) 4A4, YT33, TM71, HTA28, YG72, and alphaAIM-1. The three former antibodies revealed a particular mitotic cell cycle through site-specific phosphorylation of vimentin; that is, the early phase, mid phase, and late phase, respectively. The three later antibodies demonstrated phosphorylation of H3 at Ser28, phosphorylation of vimentin at Ser72, and aurora-B, respectively, making it possible to identify aurora-B distribution and function during mitosis. In addition, paraffin-embedded tissue sections obtained in three patients with giant cell glioblastoma were also examined. Multinucleated giant tumor cells immunoreacted with the mAb 4A4 and alphaAIM-1 but not with YT33, TM71, HTA28, and YG72 in vitro and in vivo. CONCLUSIONS: Findings in this study indicated that multinucleated giant tumor cells remain in the early mitotic phase because of aurora-B dysfunction, effecting aberrations in cytoplasmic cleavage without affecting nuclear division.
Subject(s)
Brain Neoplasms/metabolism , Giant Cells/enzymology , Glioblastoma/metabolism , Protein Serine-Threonine Kinases/metabolism , Antibodies, Monoclonal/metabolism , Aurora Kinase B , Aurora Kinases , Brain Neoplasms/pathology , Cell Line, Tumor , Fluorescent Antibody Technique , Giant Cells/pathology , Glioblastoma/pathology , Histones/metabolism , Humans , Mitosis , Phosphorylation , Protein Serine-Threonine Kinases/immunology , Serine/metabolism , Vimentin/metabolismABSTRACT
OBJECT: The nature and origin of multinucleated giant cells in glioma have not been made clear. To investigate the phosphorylation of intermediate filaments, the authors studied multinucleated giant cells in vitro and in vivo by using mitosis-specific phosphorylated antibodies. METHODS: Cultured human glioma cells were immunostained with monoclonal antibodies (mAbs) 4A4, KT13, and TM71, which recognized the phosphorylation of vimentin at Ser55, glial fibrillary acidic protein at Serl3, and vimentin at Ser71, respectively. Subsequently, the nature of multinucleated giant cells was investigated using laser scanning confocal microscopy. In addition, paraffin-embedded tissue sections obtained in three patients with giant cell glioblastoma were also investigated. Multinucleated giant cells were immunoreacted with the mAb 4A4 and not with KT13 and TM71 in vitro and in vivo. In addition, the authors obtained these results in multinucleated giant cells under natural conditions, without drug treatments. CONCLUSIONS: Findings in this investigation indicated that multinucleated giant cells are those remaining in mitosis between metaphase and telophase, undergoing neither fusion nor degeneration.
