Search Results

You are looking at 1 - 10 of 14 items for

  • Author or Editor: Jonathan J. Russin x
  • Refine by Access: all x
Clear All Modify Search
Free access

Jonathan Russin, David J. Fusco, and Robert F. Spetzler

We present a 25-year-old female with a history of multiple intracranial cavernous malformations complaining of vertigo. Imaging is significant for increasing size of a lesion in her left cerebellar peduncle. Given the proximity to the lateral border of the cerebellar peduncle, a retrosigmoid approach was chosen. After performing a craniotomy that exposed the transverse-sigmoid sinus junction, the dura was open and reflected. The arachnoid was sharply opened and cerebrospinal fluid was aspirated to allow the cerebellum to fall away from the petrous bone. The cerebellopontine fissure was then opened to visualize the lateral wall of the cerebellar peduncle. The cavernous malformation was entered and resected.

The video can be found here:

Free access

Brian P. Walcott, Jonathan J. Russin, Robin Babadjouni, and William J. Mack

This is the case of a man in his 40s who suffered sudden collapse into a deep coma as a result of a ruptured arteriovenous malformation (AVM) feeding artery aneurysm within the lateral ventricle. The ruptured aneurysm was successfully treated with Onyx embolization of the feeding pedicle. The AVM and the feeding artery aneurysm were then removed via a transcallosal approach. This case highlights the utility of interrogating the AVM with microcatheterization of the feeding pedicles in order to define the exact anatomical features necessary for treatment planning. It also reviews the anatomy of the choroidal fissure.

The video can be found here:

Full access

Leonardo Rangel-Castilla, M. Yashar S. Kalani, Katherine Cronk, Joseph M. Zabramski, Jonathan J. Russin, and Robert F. Spetzler


Despite advances in medical management and endovascular therapies, including the introduction of statins, antiplatelet agents, and drug-eluting stents, some patients experience medically refractory vertebrobasilar insufficiency and may benefit from robust surgical revascularization. The aim of this study was to evaluate such patients after surgical revascularization, emphasizing long-term outcomes and rates of complications.


The authors retrospectively identified 22 patients (5 women and 17 men) whose mean age was 69.1 years (range 48–81 years) who underwent revascularization of the posterior circulation via a proximal vertebral artery–carotid artery transposition between 2005 and 2013. The patients' conditions before surgery were clinically summarized, and long-term outcomes and complication rates after surgery were evaluated.


All the patients were symptomatic before surgery although they received the best medical therapy as defined by their primary care physician. Presenting symptoms consisted of stroke, transient ischemic attacks (TIAs), and/or findings attributable to posterior circulation hypoperfusion. There were no deaths associated with revascularization surgery. The postoperative complication rate was 45.5%, which included 3 cases of recurrent laryngeal nerve palsy, 1 case of thoracic duct injury, 2 cases of TIA, and 4 cases of Horner's syndrome. The thoracic duct injury was identified intraoperatively and ligated without sequelae, all the TIAs resolved within 24 hours of surgery, all 4 sympathetic plexus injuries resolved, and all but 1 of the recurrent laryngeal nerve palsies resolved, resulting in a 4.5% complication rate in a mean follow-up period of 8.8 months. All the patients had resolution of their presenting symptoms, and a single patient had symptomatic restenosis that required stenting and angioplasty, resulting in a restenosis rate of 4.5%.


Despite the optimization of medical therapies and lifestyle modifications, a select subset of patients with posterior vascular circulation insufficiency remains. In the authors' experience, vertebral artery–carotid artery transposition provides a surgical option with relatively low long-term complication and restenosis rates that are comparable or lower than those reported with endovascular treatment.

Full access

Kristine Ravina, Robert C. Rennert, Ben A. Strickland, Mark Chien, Joseph N. Carey, and Jonathan J. Russin

Moyamoya disease (MMD) is a progressive, idiopathic cerebrovascular occlusive disease. Various revascularization techniques including direct, indirect, and combined microvascular bypasses have been described. This article presents a modified revascularization technique for MMD utilizing a pedicled temporoparietal fascial flap (TPFF) for combined revascularization. This technique combines a large area of coverage for indirect revascularization with the benefits of a direct bypass. The pedicled TPFF also benefits from intact venous drainage to minimize the risk of flap swelling that could result in complications from mass effect.

Free access

Leonardo Rangel-Castilla, Jonathan J. Russin, Eduardo Martinez-del-Campo, Hector Soriano-Baron, Robert F. Spetzler, and Peter Nakaji


Arteriovenous malformations (AVMs) are classically described as congenital static lesions. However, in addition to rupturing, AVMs can undergo growth, remodeling, and regression. These phenomena are directly related to cellular, molecular, and physiological processes. Understanding these relationships is essential to direct future diagnostic and therapeutic strategies. The authors performed a search of the contemporary literature to review current information regarding the molecular and cellular biology of AVMs and how this biology will impact their potential future management.


A PubMed search was performed using the key words “genetic,” “molecular,” “brain,” “cerebral,” “arteriovenous,” “malformation,” “rupture,” “management,” “embolization,” and “radiosurgery.” Only English-language papers were considered. The reference lists of all papers selected for full-text assessment were reviewed.


Current concepts in genetic polymorphisms, growth factors, angiopoietins, apoptosis, endothelial cells, pathophysiology, clinical syndromes, medical treatment (including tetracycline and microRNA-18a), radiation therapy, endovascular embolization, and surgical treatment as they apply to AVMs are discussed.


Understanding the complex cellular biology, physiology, hemodynamics, and flow-related phenomena of AVMs is critical for defining and predicting their behavior, developing novel drug treatments, and improving endovascular and surgical therapies.

Free access

Jonathan J. Russin, Amir R. Dehdashti, Peter Vajkoczy, Satoshi Kuroda, and Ying Mao

Free access

Kristine Ravina, Ben A. Strickland, Robert C. Rennert, Joseph N. Carey, and Jonathan J. Russin

Graft stenosis and occlusion remain formidable complications in cerebral revascularization procedures, which can lead to significant morbidity and mortality. Graft vasospasm can result in early postoperative graft stenosis and occlusion and is believed to be at least partially mediated through adrenergic pathways. Despite various published treatment protocols, there is no single effective spasmolytic agent. Multiple factors, including anatomical and physiological variability in revascularization conduits, patient age, and comorbidities, have been associated with graft vasospasm pathogenesis and response to spasmolytics. The ideal spasmolytic agent thus likely needs to target multiple pathways to exert a generalizable therapeutic effect. Botulinum toxin (BTX)–A is a powerful neurotoxin widely used in clinical practice for the treatment of a variety of spastic conditions. Although its commonly described paradigm of cholinergic neural transmission blockade has been widely accepted, evidence for other mechanisms of action including inhibition of adrenergic transmission have been described in animal studies. Recently, the first pilot study demonstrating clinical use of BTX-A for cerebral revascularization graft spasm prevention has been reported. In this review, the mechanistic basis and potential future clinical role of BTX-A in graft vasospasm prevention is discussed.

Full access

Ben A. Strickland, Robert C. Rennert, Joshua Bakhsheshian, Sebina Bulic, Adrian J. Correa, Arun Amar, Joseph Carey, and Jonathan J. Russin

Surgical revascularization continues to play an important role in the management of complex intracranial aneurysms and ischemic cerebrovascular disease. Graft spasm is a common complication of bypass procedures and can result in ischemia or graft thrombosis. The authors here report on the first clinical use of botulinum toxin to prevent graft spasm following extracranial-intracranial (EC-IC) bypass. This technique was used in 3 EC-IC bypass surgeries, 2 for symptomatic carotid artery occlusions and 1 for a ruptured basilar tip aneurysm. In all 3 cases, the harvested graft was treated ex vivo with botulinum toxin before the anastomosis was performed. Post-bypass vascular imaging demonstrated patency and the absence of spasm in all grafts. Histopathological analyses of treated vessels did not show any immediate endothelial or vessel wall damage. Postoperative angiograms were without graft spasm in all cases. Botulinum toxin may be a reasonable option for preventing graft spasm and maintaining patency in cerebral revascularization procedures.

Full access

Kristine Ravina, Ben A. Strickland, Robert C. Rennert, Vance Fredrickson, Joshua Bakhsheshian, Mark Chien, William Mack, Arun Amar, and Jonathan J. Russin

Fusiform aneurysms of the vertebral artery (VA) involving the posterior inferior cerebellar artery (PICA) origin are uncommon and challenging. The anterior spinal artery (ASA) commonly originates from a unilateral ramus just distal to the PICA. Occlusion of an unpaired ASA can result in bilateral medial medullary syndrome. The authors propose a treatment paradigm for ASA preservation based on the artery’s proximity to fusiform VA aneurysms, and they present 3 representative cases. In the first case, they performed a V3-PICA bypass using an interposition graft and then performed endovascular coil embolization of the parent VA. A complete occlusion of the aneurysm and VA was complicated by ASA thrombosis. The subsequent cases were treated with PICA-PICA bypass and subsequent endovascular embolization of the VA. Filling of the sole angiographic ASA remote from the aneurysm was preserved in both cases. The anatomy of the ASA is the most critical determinant of treatment recommendations for fusiform VA aneurysms involving PICA. When the ASA originates from the aneurysm, proximal occlusion with or without a PICA bypass is suggested. In cases in which the ASA is removed from the aneurysm, the authors recommend revascularization followed by endovascular sacrifice. When the aneurysm is immediately adjacent to the ASA, revascularization and open trapping should be considered.

Free access

Jonathan J. Russin, Robert F. Spetzler, Steven Giannotta, Fredric B. Meyer, Michael T. Lawton, and Aaron A. Cohen-Gadol