Kenichi Haraguchi

Mechanism of the formation of dural arteriovenous fistula: the role of the emissary vein.

Dural arteriovenous fistula (DAVF) can be separated into two types: DAVF which drains through an affected sinus (sinus type) and DAVF with direct reflux to the cortical vein (non-sinus type). The present report attempted to clarify the mechanism of formation and development of DAVF focusing on the emissary vein (EV) hypothesis. First, inflammation occurs at the penetrating point of the EV on the dura due to idiopathic or secondary causes. Local inflammatory reactions induce vessel dilatation and neovascularization, and subsequently create arteriovenous (AV) connections on the arteriole level. Although EV communicating with dural arteries might play a role as draining routes at first, they start to degrade due to compression of enlarged emissary arteries or to a hemodynamic shift to the drainage pathway of least resistance. Following the occlusion of drainage pathway through EV into the sinus or cortical veins may form, resulting in clinically detectable DAVF. The AV shunt then expands to the surrounding dura associated with recruitment of feeders from distant sites induced by expression of angiogenetic factors and a shift in the hemodynamic balance. In sinus type DAVF, the sinus is progressively compartmentalized and finally occludes due to thrombogenesis with activated coagulopathy or to hemodynamic hypertrophy of the sinus wall. This progression results in the mature, aggressive DAVF with drainage impairments. Previous mechanistic hypotheses focusing on sinus hypertension and sinus thromboses cannot explain the pathogenesis of non-sinus type of DAVF. Although the etiology of DAVF may be concerned by the thrombo-occlusive change of sinus, the unique theory presented in this report may enable an understanding of the common etiology of both types of DAVF.

Magnetic resonance fluid dynamics for intracranial aneurysms—comparison with computed fluid dynamics

BackgroundHemodynamics in intracranial aneurysms is thought to play an important role in their growth and rupture. Usual computed fluid dynamics (CFD) based on three-dimensional (3D) computed tomographic (CT) angiography requires a time-consuming process for analysis. Magnetic resonance fluid dynamics (MRFD) based on MR images is a new tool for analyzing flow dynamics and a promising method for obtaining such information more easily. We compared the data from MRFD and CFD and studied the clinical feasibility of MRFD.MethodsA total of 15 aneurysms, including two ruptured ones, in 15 patients were investigated with MR imaging and 3D-CT angiography. The flow data of MRFD and CFD, 3D stream lines, flow velocity profile and wall shear stress (WSS) were extracted from the image reconstruction and were compared each other.ResultsBoth flow dynamics images showed quite similar 3D flow pattern and WSS map. However, the calculated value of maximum WSS was quite different and there was no significant correlation. Further, in one ruptured case, CFD showed less visualization to evaluate the intra-aneurysmal flow. Interestingly, one delayed rupture case showed a particular flow pattern with abnormal secondary flow in the bottom of the aneurysm before rupture, which might suggest the specific finding of rupture risk.ConclusionMRFD is a valuable and less invasive tool to evaluate aneurysmal fluid dynamics. It can be obtained from the usual MRI examination without contrast medium and exposure to radiation. Although there is a problem of consistency of the absolute value of WSS between MRFD and conventional CFD, it may be useful to predict the risk of enlargement or rupture of aneurysms based on the information of the similar distribution of WSS and flow patterns. The quantifiable analysis and establishment of a meaningful threshold for high risk should be further studied.

Fenestration of a supraclinoid internal carotid artery associated with dual aneurysms: case report.

BACKGROUND AND IMPORTANCE:We present a rare case of fenestration of the left supraclinoid intracranial internal carotid artery with 2 associated aneurysms arising proximally and distally from the fenestration that were successfully treated with endovascular coil embolization. This is the first report of these types of aneurysms treated with coiling alone. CLINICAL PRESENTATION:A 47-year-old woman underwent a diagnostic workup; magnetic resonance angiography incidentally revealed 2 tandem aneurysms at the supraclinoid and paraclinoid portion of the left internal carotid artery. Angiography revealed fenestration of the left supraclinoid internal carotid artery with 2 aneurysms both proximal and distal to the fenestration. The patient underwent endovascular coil embolization of the aneurysms simultaneously. The smaller trunk was intentionally occluded to achieve complete packing of the proximal aneurysm. Both aneurysms were totally occluded, and no neurological deficits developed in the patient. CONCLUSION:Based on previous reports, fenestration has the potential to form an aneurysm, and there seemed to be a relatively high incidence of rupture if accompanied by aneurysm. Coiling is one good option to treat aneurysms and should be considered when multiple aneurysms exist because all aneurysms can be treated simultaneously. Proximal occlusion of the smaller trunk is acceptable because of a retrograde flow from the distal end, even if one exists.

The mechanism of catheter kickback in the final stage of coil embolization for aneurysms: the straightening phenomenon.

The catheter kickback phenomenon often occurs in the last stage of coil packing for cerebral aneurysms. This behavior is considered the result of either a lack of space in the sac or a stiff detaching zone. In order to clarify its mechanism, focused stretch-resistance (SR) coil simulation models were tested. Various commercially available SR coils were inserted into a cylinder or an aneurismal sac made from a silicone tube with a smaller than prescribed diameter. A magnified SR coil model (straight type) of fishing line was created for simulation. Numerical analysis for the changes in coil behavior were verified. All SR coils showed hardening and straightening at the last few millimeters, resulting in catheter kickback. In a magnified coil experiment, straightening was also realized when folding into a narrow cylinder. The SR line coursed in the canal of the first loops and shifted to the outside in the middle portion. Gaps among first coil pitches were enlarged on after insertion into the narrower space. Shortage of the SR line was calculated to reach a maximum of 32%. The straightening phenomenon is due to SR line shortening and subsequent condensation of pitches of the first loops at the coil end. Coil tail flexibility was lost, and the coil behaved as a stiff wire. Straightening is an important factor in the kickback phenomenon. Shorter final SR coils should be selected, and coil designs should be improved.

Relationship between low response to clopidogrel and periprocedural ischemic events with coil embolization for intracranial aneurysms

Objectives Low response to antiplatelet drugs is one of the risk factors for ischemic events. We examined the influence of low response to clopidogrel on symptomatic ischemic events and new ischemic MRI lesions with endovascular intracranial aneurysmal coil embolization. Materials and methods Between August 2010 and July 2013, 189 procedures in 181 consecutive patients who underwent endovascular coiling and received clopidogrel before treatment were investigated retrospectively. Platelet aggregation activity was examined by VerifyNow analysis. Low response to clopidogrel was defined as P2Y12 reaction units ≥230 in this study. Symptomatic ischemic complications within 30 days and postoperative new ischemic lesions on MRI–diffusion weighted imaging were evaluated. Results 66 of 189 (34.9%) cases were low responders to clopidogrel. Ischemic complications occurred in 2 of 66 (3.0%) low responders compared with 6 of 123 (4.9%) responders (p=0.72). A new high intensity spot larger than 5 mm was significantly more frequent in low responders (26 of 66; 39.4%) than in responders (26 of 121; 21.2%; p=0.01). On multivariate analysis, independent risk factors for larger new ischemic lesions were low response to clopidogrel, smokers, posterior location, and aneurysms with a larger neck. Conclusions Low response to clopidogrel had little effect on clinical outcome although it increased asymptomatic large ischemic lesions in this cohort.

Pial arteriovenous fistula as a cause of bilateral thalamic hyperintensities--an unusual case report and review of the literature.

INTRODUCTION Isolated bilateral thalamic congestion due to an arteriovenous malformation (AVM) is a rare entity. Few case reports of dural arteriovenous fistula associated with it have been reported in the literature. The association of pial arteriovenous fistula (pial AVF) with thalamic hyperintensities has never been described before. The pial AVF is a recently recognized lesion in which the multiple pial arterial feeders drain into a single venous channel without a nidus like in conventional AVM. In spite of being congenital in origin, these lesions may have expression in adulthood due to abrupt change in the venous drainage system. Successful management of pial AVF associated with bilateral thalamic hyperintensities is described here with review of the literature. CASE PRESENTATION A 60-year-old man presented with rapidly progressive gait disturbance and cognitive decline. Magnetic resonance imaging (MRI) showed hyperintensities in the thalami on T2-weighted and fluid attenuated inversion recovery image. Digital subtraction angiography revealed a pial AVF near the splenium of corpus callosum. It had feeders from posterior choroidal arteries and drained into the vein of Galen through an abnormal mesencephalic vein. The stagnation and increase of pressure in the deep venous system led to congestion in the thalami. He was treated by partial transarterial embolization of the feeders followed by gamma knife therapy (GKT). The clinical symptoms and MRI improved rapidly after embolization and further reduction in shunt flow was observed after GKT. CONCLUSION Strong suspicion of vascular malformation as a cause of bilateral thalamic hyperintensities helps in early detection. Such lesions like pial AVF presented here require active intervention by surgery or endovascular therapy. GKT is an important adjuvant in lesions refractory to either of them.

A unique type of dural arteriovenous fistula at confluence of sinuses treated with endovascular embolization: a case report.

Dural arteriovenous fistula (DAVF) is classically defined as abnormal arteriovenous connections located within the dural leaflets. Though the exact etiology is still not clear, they are generally accepted as acquired lesions. However, some DAVFs formed as the congenital disorders are called dural arteriovenous malformations and these lesions with a marked cortical venous reflux are considered to be aggressive and warrant an early intervention. The authors describe a case of 35-year-old man presented with unique type of DAVF. The fistula was located adjacent to the confluence of venous sinuses with multiple feeders. The feeders drained into a large venous pouch just anterior to the confluence which had a bilateral venous drainage. This was associated with multiple cerebellar venous ectasia along the draining cortical vein. It was managed by staged endovascular procedures and complete cure could be achieved. The pathogenesis and technique of embolization of this complex fistula/malformation are also discussed.