Brain Protection for Cerebral Aneurysm Surgery

Knowledge about the cellular physiology of cerebral ischemia is expanding rapidly, and we stand at the edge of a new age in which clinicians are able to directly intervene in these processes. Experience from the recent clinical trials using recominant tissue plasminogen activator emphasizes that urgent intervention is necessary. Furthermore, recent studies in animal models of middle cerebral artery occlusion demonstrate that between 40% and 50% of ischemic tissue can potentially be salvaged up to 2 hours after ischemia. Ongoing studies with NMDA receptor antagonists, free radical scavengers, calcium channel blockers, and other innovative therapies should identify which agents are effective in limiting the deleterious effects of the ischemic cascade and rescuing the ischemic penumbra. The neurosurgeon is in the enviable position of being able to benefit from advances in ischemic research, in part, because the neurovascular surgeon can institute protective measures prophylactically before the onset of ischemic insult. Until new and effective therapies become available, the risks of ischemia in the operating room can be reduced by careful attention to normal physiological processes, including blood pressure, oxygenation, and glucose levels as well as the judicious use of barbiturates and hypothermia

Surgical Management of Large AVMS

The surgical management of large AVMs (those greater than 6 cm in maximal diameter) should be based on a thorough understanding of the chronic hemodynamic changes produced by lesions and the acute stress placed on the cerebral vasculature by their removal. In addition to haemorrhage, seizure, and headache, these larger lesions often present with symptoms of cerebral vascular insufficiency. Angiography frequently demonstrates a high-flow arteriovenous shunt with evidence of vascular steal from the surrounding brain. In many cases there is a virtual absence of normal hemispheric filling. When the steal is sufficient to produce an area of chronic ischaemia in the brain surrounding the AVM, there is an increased risk of swelling and haemorrhage associated with complete excision. We have developed a strategy for the surgical management of these large lesions that involves a stepwise reduction of flow through the AVM using pre- and intraoperative embolization, followed by complete excision. The details of this management strategy are described, and results in 24 patients with exceptionally large AVMs are presented

Dural Arteriovenous Fistula of the Transverse-Sigmoid Sinus Causing Trigeminal Neuralgia

The authors analysed an unusual case of dural arteriovenous fistula (DAVF) of the transverse-sigmoid sinus causing trigeminal neuralgia is presented. Although progression to almost continuous facial pain has been reported, symptoms may be indistinguishable from typical trigeminal neuralgia. The patient had a 6-year history of right-sided trigeminal neuralgia initially well controlled by medical management. He was referred for surgical management after 10 months of progressively worsening of symptoms. At the time of consultation, the patient complained of pulsatile tinnitus in the right ear. Computed tomography imaging and angiography demonstrated a DAVF involving the right transverse-sigmoid sinus junction with retrograde venous drainage. Surgical resection of the DAVF provided both angiographic cure and complete relief of all symptoms. The authors discuss the pathophysiology of trigeminal neuralgia in patients with a DAVF. © 2007 Springer-Verlag

Simplified Aqueductal Stenting for Isolated Fourth Ventricle Using a Small-Caliber Flexible Endoscope in a Patient With Neurococcidiomycosis: Technical Case Report

Endoscopic aqueductoplasty and stenting are a preferred treatment for isolated fourth ventricle syndrome related to membranous aqueductal obstruction. We describe a technique using a small-caliber flexible endoscope that may address some limitations of current strategies. A 39-year-old woman with hydrocephalus caused by neurococcidiomycosis and a functional right frontal ventriculoperitoneal shunt presented with vomiting and an isolated fourth ventricle. Magnetic resonance imaging showed an enlarged fourth ventricle and exuberant basilar arachnoiditis obstructing the outlet foramina of the fourth ventricle. Ventriculography indicated aqueductal obstruction. Aqueductoplasty was planned to allow spinal fluid to flow from the fourth ventricle to the ventriculoperitoneal shunt. A stent-endoscope construct was prepared by feeding a flexible endoscope through a ventricular catheter cut 4 cm from the tip. The flexible endoscope was contoured to fit the anatomy of the aqueduct. Uncomplicated aqueductoplasty was performed through a single left frontal burr hole using the stent-endoscope construct to perforate a membranous veil and inspect the fourth ventricle. The stent was deployed over the endoscope using the proximal end of the catheter to deliver and secure the stent as the endoscope was withdrawn. Aqueductoplasty and stenting using a small-caliber flexible endoscope is feasible. The endoscope can be contoured to suit the anatomy of the aqueduct and improves visualization of the leading edge of the stent during deployment. Furthermore, when the endoscope is used to create the perforation, the target is not obscured by the shaft of the device used to make the perforation

Rupture of a Previously Documented Small Asymptomatic Intracranial Aneurysm in a Patient With Autosomal Dominant Polycystic Kidney Disease

Intracranial aneurysms are common extrarenal manifestations of autosomal dominant polycystic kidney disease (ADPKD). Although their natural history is not completely understood, small asymptomatic intracranial aneurysms in patients with ADPKD often are not treated but are followed with serial magnetic resonance (MR) angiography. The authors report the unique case of a patient with ADPKD who bled from a previously documented asymptomatic 3-mm intracranial aneurysm. This 42-year-old man with ADPKD suffered a subarachnoid hemorrhage (SAH) from a 7-mm left pericallosal artery aneurysm. This aneurysm was clipped and the patient made an excellent recovery. An irregular asymptomatic 3-mm right middle cerebral artery (MCA) aneurysm had also been demonstrated on angiography. While the patient was considering elective surgery for the MCA aneurysm, he suffered a hemorrhage from this lesion 10 weeks after the initial SAH. The aneurysm was clipped and the patient made a satisfactory recovery (he was moderately disabled). In this report the authors indicate that small asymptomatic intracranial aneurysms are not always innocuous in patients with ADPKD, and they suggest that treatment should be strongly considered for these lesions in this group of patients when there is a history of SAH or the aneurysm is irregular in appearance. Because MR angiography studies may not adequately define the configuration of small aneurysms and irregularity may easily be missed, conventional angiography is recommended for patients with ADPKD who are found to have an intracranial aneurysm on screening with MR angiography

Reversed-Flow Saphenous Vein Grafts for Cerebral Revascularization: Technical Note

The authors sought to create a saphenous vein interposition graft to be used in cerebral bypass procedures that would be more physiologically appropriate than standard vein grafts and would provide a better match between the graft and recipient vessels at the anastomotic sites. The saphenous vein graft was prepared by lysing the valves with a valvulotome. The blood flow could then be reversed in the vein, allowing it to be used in either direction as a bypass graft. An illustrative case including angiograms that con finn good patency and blood flow through the reversed-flow bypass graft is presented. It is concluded that the reversed-flow saphenous vein graft provides a more physiologically suitable conduit than standard vein grafts. Lysis of the valves allows the graft to be used in an orientation that takes advantage of the natural tapering of the vein to produce a better match with the recipient vessels at the anastomotic sites. Minimizing diameter changes at the proximal and distal anastomoses helps reduce turbulence, which has been implicated as a cause of early graft failure and thrombosis

Microvascular Decompression After Gamma Knife Surgery for Trigeminal Neuralgia: Intraoperative Findings and Treatment Outcomes

Object. The authors sought to determine whether the results of trigeminal microvascular decompression (MVD) are influenced by prior gamma knife surgery (GKS). Methods. Gamma knife surgery is an established procedure for treating medically intractable trigeminal neuralgia but failures do occur. The authors assessed six patients (two men and four women; mean age 52 years) who experienced pain recurrence after GKS and elected to undergo trigeminal MVD via retrosigmoid craniotomy. Three patients underwent a single GKS to a maximal dose of 80 Gy, whereas three others underwent a second GKS to total of 120 to 135 Gy. At surgery, none of the six patients demonstrated excess arachnoid thickening, grossly apparent changes in the nerve itself, or any other tissue alterations that made successful mobilization of a blood vessel from the trigeminal root entry zone technically more difficult. A single individual had a small atherosclerotic plaque in the superior cerebellar artery near its contact point with the trigeminal nerve. Follow up at a mean of 25.4 months (range 7.5-42 months) indicated that five patients were pain free. One patient had improved but still relied on medications for pain control. Conclusions. In the authors\u27 experience, trigeminal MVD can be performed without added difficulty in patients who have previously undergone GKS. The success rates seem similar to those normally associated with MVD. Patients who elect the less invasive option of GKS can be assured that trigeminal MVD remains a viable alternative at a later date if further surgery is required

Superficial Temporal Artery-To-Middle Cerebral Artery Bypass Grafting for Cerebral Revascularization

SUPERFICIAL TEMPORAL ARTERY-to-middle cerebral artery bypass procedures are an important toot in the armamentarium of cerebrovascular surgeons for the treatment of carotid occlusion and revascularization for complex aneurysms and brain tumors. This article enumerates the essential steps in performing superficial temporal artery-to-middle cerebral artery bypass procedures. The nuances of this technique reflect the extensive experience of the senior authors (RFS, JMZ)

Improved Transdural Exposure and Temporary Occlusion of the Petrous Internal Carotid Artery for Cavernous Sinus Surgery: Technical Note

Safe surgery for vascular and neoplastic lesions involving the cavernous sinus requires adequate proximal control of the cavernous internal carotid artery (ICA). Classically, control of the cavernous ICA has necessitated dissection and isolation of the cervical vessels. The authors describe an alternative method for obtaining vascular control via transdural exposure of the petrous ICA and the use of the Fogarty balloon embolectomy catheter inserted extra-arterially into the carotid canal to provide temporary occlusion. This method is particularly well suited for proximal ICA occlusion during short-segment petrous-to-paraclinoid ICA bypass procedures as it eliminates the need for a temporary proximal ICA aneurysm clip and increases the available working space for completion of the anastomosis

Cavernous Malformations: Genetics Molecular Biology and Familial Forms

Cavernous malformations are compact lesions composed of sinusoidal vascular channels that resemble dilated capillaries. They are found throughout the central nervous system with an estimated incidence in the general population of about 0.4%. Cavernous malformations occur as a sporadic form in which lesions tend to be solitary and as a familial form characterized by multiple lesions and a strong family history of seizures. The familial forms of this disease are inherited in an autosomal dominant mode. Genetic studies have identified three distinct loci associated with the familial forms of this disease - which have been termed cerebral cavernous malformations (CCM): CCM1 located on the long arm of chromosome 7 (7q21 to 7q22), CCM2 on the short arm of chromosome 7 (7p13-p15), and CCM3 on the long arm of chromosome 3 (3q25 to 3q27). In the CCM population, 40% of families link to CCM1, 20% to CCM2, and 40% to CCM3. Further analysis has demonstrated that mutations in the KRIT1 gene are responsible for CCM1. KRIT1 is a binding protein that interacts with Krev-1/rap1a, a member of the Ras family of GTPases with tumor-suppressing activity for the Ras oncogenes. These findings, along with the evidence from magnetic resonance imaging (MRI) studies that the de novo appearance of new lesions is relatively common, suggest that cavernous malformations should be reclassified as benign vascular tumors. 2002, Elsevier Science (USA). All rights reserved