[Contribution of increasing age to carotid plaque morphology and symptoms].

OBJECTIVE: Aging is considered to cause atherosclerotic changes in the carotid artery, but few studies have evaluated this relationship. In this study, we used carotid plaques removed from patients with carotid artery stenosis and investigated how aging contributes to carotid plaque morphology and symptoms. MATERIALS AND METHODS: A total of 60 patients(55 men, 5 women; mean age, 70.5 years; range, 53-85 years) treated at our hospital between January 2009 and April 2012 were enrolled in this study. All patients underwent carotid endarterectomy; their carotid plaques were stained with hematoxylin-eosin and/or Elastica-Masson stain and examined by a pathologist. Using these data, the carotid systolic velocity and plaque morphology were analyzed considering the age by decade as well as the symptomatology. RESULTS: Of the 60 patients, 29 were symptomatic(transient ischemic attack (TIA) in 8 patients; infarction in 20;and amaurosis in 1). Symptoms were less common as patient age increased. The incidence of TIA also tended to decrease with an increase in age, although the opposite trend was seen with infarction. In plaque morphology, the presence of active plaque, macrophage, inflammatory infiltration, and capillary angiogenesis decreased as age increased, while the presence of degenerative plaques, decrease in smooth muscle cell number, and calcification inversely increased. Active, degenerative, and combined (active/degenerative) lesions are statistically unrelated to symptoms as well as systolic velocity (cm/sec) at the carotid stenosis. The rates of hemorrhagic lesions were similar among decades, but the lesion statistically contributed to increasing symptoms (p=0.0045) and increasing systolic velocity (p=0.031). CONCLUSION: Increasing age contributes to morphological changes in carotid plaques and symptoms. When hemorrhagic lesions are suspected in carotid plaques, patients will be symptomatic and may require surgery.

Role of magnetic resonance vessel wall imaging in detecting and managing ruptured aneurysms among multiple intracranial aneurysms.

BACKGROUND: Wall enhancement of intracranial saccular aneurysms in high-resolution magnetic resonance vessel wall imaging (MR-VWI) might indicate a ruptured aneurysm. Therefore, this study aimed to determine the diagnostic ability of wall enhancement to detect the ruptured aneurysms among multiple aneurysms. METHODS: Patients with subarachnoid hemorrhage (SAH) and multiple intracranial aneurysms who underwent MR-VWI before craniotomy and clipping were included in the study. Three-dimensional T1-weighted fast spin-echo sequences were obtained before and after gadolinium injection. Aneurysm rupture was estimated based on the subarachnoid clot distribution, aneurysmal contours, and MR-VWI findings. We selectively performed surgical clipping and confirmed the rupture site intraoperatively. RESULTS: Thirteen patients with SAH with 13 ruptured and 17 unruptured aneurysms were treated at out facility. The accuracy rate of rupture site diagnosis using MR-VWI was 69.2% (9/13 cases). Each unruptured aneurysm was equally or more strongly enhanced in the other four cases than the ruptured aneurysms. In three of the four unruptured aneurysms with positive MR-VWI findings, atherosclerosis of the aneurysmal wall was observed during simultaneous or elective clipping surgery. Further, clipping surgery was performed without intraoperative rupture in two cases with the help of MR-VWI findings. CONCLUSION: Correct diagnosis of the rupture site using MR-VWI alone was unreliable due to false positives caused by the wall enhancement of unruptured aneurysms with atherosclerosis. Therefore, ruptured aneurysms should be detected using more information in addition to MR-VWI images. MR-VWI may be advantageous to determine surgical strategies when managing patients with SAH and multiple aneurysms.

A case of falcine sinus dural arteriovenous fistula.

BACKGROUND AND IMPORTANCE: The falcine sinus is an embryonic vessel that connects the superior and inferior sagittal sinuses and mostly closes after birth. Although some cases of persistent falcine sinus have been reported, dural arteriovenous fistula (dAVF) associated with the falcine sinus has not previously been reported. CLINICAL PRESENTATION: A 60-year-old man presented with asymptomatic dAVFs on digital subtraction angiography. The dAVFs were fed mainly by the cortical branch of the left anterior cerebral artery and drained into the falcine sinus. Intraoperatively, all veins draining in a retrograde manner into cortical veins were obstructed. However, cortical venous reflux did not disappear before removal of the falx cerebri, including the falcine sinus and inferior sagittal sinus. In this case, we considered falcine sinus dAVF as equivalent to olfactory groove dAVF because the medial olfactory artery, in its role as a common feeding artery in olfactory groove dAVF, is a rudiment of the anterior cerebral artery as the main feeding artery in this case. Intraoperative findings and the surgical specimen revealed a small vessel network in the falx cerebri communicating with the falcine and inferior sagittal sinuses, which was considered to represent a falcine venous plexus, not a vessel anomaly. CONCLUSION: Extensive removal of the falx cerebri including the falcine sinus or complete endovascular obliteration of the whole falcine sinus as early as possible represents an important strategy in the surgical treatment of falcine sinus dAVF.