Endovascular Management of a Ruptured Aneurysm on a Posterior Inferior Cerebellar Artery with Extradural C2-Origin: Case Report and Literature Review.

Extracranial vascular pathology uncommonly causes intracranial subarachnoid hemorrhage (SAH). Among possible lesions are aneurysms at the craniocervical junction arising from a posterior inferior cerebellar artery (PICA) with an extradural origin. We describe a case of a 55-year-old female presenting with a sudden and severe headache. A computed tomography scan revealed a SAH within the fourth ventricle and cervical spinal canal, and a ruptured saccular aneurysm on a PICA with extradural C2-origin. Despite difficult access anatomy, endovascular treatment was feasible and resulted in subtotal initial occlusion and preservation of distal PICA flow. Upon 3-month follow-up, the aneurysm was completely occluded with a patent PICA. The patient's clinical status remained stable at the 1.5-year follow-up. In conclusion, we present a rare case of an aneurysm originating from a PICA with extradural C2-origin that was treated endovascularly with preservation of the PICA.

Vertebro-Vertebral Fistula Occlusion Using a Woven EndoBridgeTM-Device.

Vertebro-vertebral fistulas (VVFs) are vascular lesions that may develop after trauma or spontaneously in association with connective tissue disorders. We present a rare case of a post-traumatic VVF in a young patient presenting with a painless swelling and a bruit in her left upper neck. Digital subtraction angiography showed an arteriovenous fistula between the left vertebral artery (VA) and the vertebral venous plexus with significant steal phenomenon. Endovascular therapy was performed using a Woven EndoBridgeTM (WEB)-device combined with coils that allowed preservation of the VA. The patient fully recovered from her symptoms and follow-up imaging showed stable occlusion. In conclusion, VVFs can be effectively treated using intrasaccular flow diverters such as the WEB-device, allowing for complete and stable occlusion while preserving the parent artery.

Endovascular occlusion of a persistent stapedial artery prior to stapedotomy: a novel approach.

BACKGROUND: The stapedial artery is an embryonic artery that transiently supplies the cranial vasculature of the human embryo. Postnatal persistence of the stapedial artery may cause conductive hearing loss and pulsatile tinnitus due to its course through the middle ear. We describe a patient with a persistent stapedial artery (PSA) managed by endovascular coil occlusion prior to stapedotomy. METHODS: A 48-year-old woman presented with left-sided conductive hearing loss and pulsatile tinnitus. Ten years earlier the patient had undergone explorative tympanoplasty, which was aborted due to a large PSA. Digital subtraction angiography was performed to confirm the anatomy and endovascular occlusion of the proximal PSA was achieved by deployment of coils. RESULTS: The pulsatile tinnitus improved immediately after the procedure. The size of the artery subsequently decreased and surgery could be performed with only a minor intraoperative bleeding. Successful stapedotomy resulted in postoperative normalization of her hearing with some minor residual tinnitus. CONCLUSION: Endovascular coil occlusion of a PSA is feasible and safe in patients with favorable anatomy and facilitates middle ear surgery. It decreases the size of the artery and minimizes the risk of intraoperative bleeding in patients with a large PSA. The future role of this novel technique in the management of patients with PSA-related conductive hearing loss and pulsatile tinnitus remains to be determined.

Fragmentation of Hydrophilic Guidewire Coatings During Neuroendovascular Therapy.

PURPOSE: Cerebral polymer coating embolism from intravascular devices may cause serious complications after endovascular therapy (EVT) for neurovascular diseases. Although polymer fragments are often created during endovascular procedures, exact mechanisms of their formation, especially if of small size, are largely unknown. METHODS: In this study eight microguidewires (Asahi Chikai 200 cm (Asahi Intecc, Aichi, Japan), Asahi Chikai Black (Asahi Intecc), Fathom™ (Boston Scientific, Marlborough, MA, USA), Hybrid (Balt Extrusion, Montmorency, France), Radifocus® Guide Wire GT (Terumo, Leuven, Belgium), Synchro2® (Stryker, Kalamazoo, MI, USA), Transend™ EX (Boston Scientific), and Traxcess™ (MicroVention®, Tustin, CA, USA)) frequently used during EVT were investigated ex vivo using their dedicated metal or plastic insertion tools to assess for coating delamination after backloading of the microguidewires. RESULTS: Backloading caused damage to the coating of all microguidewires especially when the main body of the guidewires was bent in front of the insertion tool. All studied microguidewires produced microscopic filamentous and/or band-like coating fragments. Few larger irregular fragments were observed, but also very small fragments measuring 1-3 µm in diameter were found. Spectroscopic measurements of polymer fragments and microguidewires identified various polymers. CONCLUSION: Backloading of polymer-coated microguidewires during EVT should be minimized if possible. More stable hydrophilic coatings on microguidewires and less traumatic insertion tools are desirable.

Dissecting pseudoaneurysm in a spinal cord AVM treated by flow diversion: Technical note.

We report the case of a 29-year-old woman presenting with severe back pain and S1-radiculopathy. Digital subtraction angiography revealed a spinal cord arteriovenous malformation complicated by acute feeder dissection and pseudoaneurysm (PA) formation causing mass effect. After conservative management with limited angiographic and clinical improvement, selective treatment of the PA by flow diversion (FD) led to occlusion and shrinkage with the resolution of clinical symptoms. FD may be a feasible treatment option for spinal artery aneurysms in selected patients with favorable anatomy. The need for antiplatelet therapy is a limitation of its use with currently available devices.

Hemorrhage due to a pseudoaneurysm on a dural-pial anastomosis after decompression for Chiari malformation type I: case report.

While intracranial aneurysms rarely develop after neurosurgical procedures, delayed pseudoaneurysm formation after foramen magnum decompression (FMD) has never been reported. A 52-year-old woman presented with an atypical subarachnoid hemorrhage in the posterior fossa 12 years after a FMD for symptomatic Chiari malformation type I was performed. A pseudoaneurysm on a dural-pial anastomosis was identified as the bleeding source and successfully occluded by endovascular means with full clinical recovery of the patient. Injury to the distal posterior inferior cerebellar artery related to surgery and postoperative infection likely caused formation of a dural-pial anastomosis. Additionally, hemodynamic stress or dissection may have contributed to delayed pseudoaneurysm formation and rupture.

Polytetrafluoroethylene coating fragments during neuroendovascular therapy: An analysis of two damaged microguidewires.

Cerebral polymer coating embolism from intravascular devices represents a potentially serious complication to endovascular therapy (EVT). We report two cases of neuroendovascular treatment where filamentous polymer fragments were noted possibly due to damage of the surface coating during manipulation and backloading of microguidewires. As the exact origin of the debris was initially not known, microguidewires and fragments were examined with light microscopy, stereomicroscopy, scanning electron microscopy and attenuated-total-reflection Fourier transform infrared spectroscopy. Fragments consisted of polytetrafluoroethylene and silicone oil stemming from the proximal shaft of a standard microguidewire. To our knowledge, this is the first report of polytetrafluoroethylene coating fragments created during EVT. Future studies should assess the mechanism of polymer coating delamination and its potential consequences during EVT including inadvertent fragment migration into the cerebral circulation.

Alternative route to a hypoglossal canal dural arteriovenous fistula in case of failed jugular vein approach.

Hypoglossal canal dural arteriovenous fistulas (HC-DAVF) involve the anterior condylar vein (ACV) and anterior condylar confluence (ACC). They often present with tinnitus, bruit, and hypoglossal nerve palsy. The most common treatment in HC-DAVFs is transvenous embolization using coils and the most direct transvenous route is the trans-internal jugular vein access. When this approach is not feasible, a treatment attempt is possible through alternative routes. We report 2 patients with DAVFs involving the anterior condylar confluence. The first patient presented with pulsatile tinnitus and hypoglossal nerve palsy, and was treated by a standard transjugular approach. The second patient presented with pulse-synchronous bruit. Following an unsuccessful attempt of the transjugular approach, the fistulous point was reached via the deep cervical vein and complete occlusion was achieved by coil deployment. Both patients had complete regression of symptoms. Endovascular therapy is the elective treatment for HC-DAVFs and the transjugular approach is the most commonly used. The deep cervical vein (DCV) can be an alternative transvenous route when the transjugular approach fails.

Dural Arteriovenous Fistula of the Vein of Trolard Mimicking a Cavernous Sinus Fistula.

BACKGROUND: Arteriovenous fistulas (AVFs) involving the cavernous sinus usually become clinically apparent due to eye symptoms. Although rare, the same symptoms can be associated with AVFs located remote from the cavernous sinus when the shunt drains into its tributaries. We report the unusual case of a dural AVF in which such communication was not immediately obvious from the diagnostic angiogram. CASE DESCRIPTION: A 61-year-old male presented with increasing lid swelling, proptosis, and redness of the right eye for 1 month. Digital subtraction angiography showed no evidence of a cavernous sinus fistula but revealed a dural AVF between the right middle meningeal artery and the vein of Trolard. The fistula had a minor drainage through a small superficial middle cerebral vein toward the middle cranial fossa. Late venous-phase images eventually revealed faint opacification of the right cavernous sinus and superior ophthalmic vein. Endovascular treatment was performed by transarterial embolization with complete occlusion of the AVF obtained after 2 sessions. CONCLUSIONS: Dural AVFs involving cortical veins may cause atypical symptoms suggesting a cavernous sinus fistula due to remote venous drainage. Understanding venous anatomy helps to correlate vascular pathology and clinical symptoms and thus allows efficient and safe treatment.

Subdural contrast effusion during endovascular therapy: case report.

Accumulation of contrast medium in the subdural space after diagnostic intraarterial contrast administration is a rare observation. The authors report the case of a subdural contrast effusion (SCE) presenting during endovascular treatment of an intracranial dural arteriovenous fistula (DAVF) mimicking an acute subdural hematoma. Differentiation between the two by computed tomography (CT) or intraprocedural Dyna CT and early neurological examination can be crucial for patient management. We believe that repeated large-volume contrast injections via large-bore intermediate catheters into the territory of an (even partly) occluded DAVF may induce leakage of contrast medium into the extravascular subdural space thereby causing a SCE.

A mathematical approach for assessing the transport of large neutral amino acids across the blood-brain barrier in man.

Changes in the large neutral amino acid (LNAA) transport across the blood-brain barrier (BBB) is thought to contribute to brain dysfunction in a number of clinical conditions, including phenylketonuria, acute liver failure, and sepsis. Here, we present a novel approach for estimating BBB permeability and the LNAA concentrations in brain extracellular fluid, by demonstrating that they can be mathematically derived on the basis of kinetic constants of the BBB available from the literature, if cerebral blood flow and the arterial and jugular venous LNAA concentrations are known. While it is well known that the permeability surface area product of the BBB to a LNAA from blood to brain (PS1) can be calculated from the arterial LNAA concentrations and kinetic constants of the BBB, we demonstrate that the permeability surface area product from brain to blood (PS2) can be calculated by deriving the substrate activity of the saturable transporter from the kinetic constants and arterial and jugular venous LNAA concentrations, and that the concentration of the LNAA in brain extracellular fluid can then be determined. This approach is methodically simple, and may be useful for assessing the transcerebral exchange kinetics of LNAAs in future human-experimental and clinical studies.