Epidemiology

The incidence and prevalence of intracranial aneurysms in the general population are very difficult to estimate owing to clustering in various high-risk groups, large numbers of deaths without autopsy or neuroimaging, and the presence of asymptomatic lesions. Furthermore, autopsy studies have demonstrated disparate results that do not appear to link with the prevalence of subarachnoid hemorrhages (SAHs) and rupture risk incidence. Fox¹ reviewed the autopsy literature, which spanned from 1926 to 1973, and found the rate of occurrence to be 0.8% when studies included more than 5000 cases and 2% when studies included 2 to 5000 patients. Stehbens² conducted an autopsy study between 1952 and 1954 and found at least one aneurysm in 5.6% of cadavers. In his review of the pathological literature between 1890 and 1966, the prevalence of aneurysms at autopsy was found to be approximately 2.4% with a range of 0.2% to 9%.³ Intracranial aneurysms in children are rare but are thought to occur in approximately 0.5% to 4.6%.⁴ Currently, it is thought that approximately 6% of the international population harbor intracranial aneurysms with a higher prevalence in the Asian and Finnish populations (4-9%) and those who harbor significant risk factors, such as environmental, systemic, or genetic.⁵ Risk factors associated with the presence and rupture of intracranial aneurysms have included high blood pressure, tobacco usage, and genetic- and ethnic-related factors; however, the prevalence of lesions is still thought to be approximately 2% in those without any known risk factors.⁵ Although the most prevalent risk factors are those that are modifiable, the strongest risk factors are thought to occur through genetic and familial predisposition.

The risk of intracranial aneurysm rupture has also been a controversial topic. Although the annual risk of rupture has been reported to be between 0.1 and 8%,⁵ depending on variable lesional characteristics, recent prospective data have challenged this view. The International Study of Unruptured Intracranial Aneurysms (ISUIA) reported in two recent publications^6,7 that the risk of aneurysm rupture was substantially lower than previously thought, that is, approximately 0% in anterior circulation aneurysms in those less than 7 mm, the most commonly encountered entities (Table 13.1). Although these studies represented the largest prospective collection of data regarding unruptured aneurysms, they have also been met with intense scrutiny and controversy, especially in light of a multitude of studies reporting an order of magnitude greater rupture risk.⁸ Common problems with estimating the annual rupture risk are the inclusion of all patients with aneurysms, regardless of presentation, proper lesion classification and grouping, taking into account specific lesional characteristics, and proper classification of patients into various risk groups.⁸ Given the broad spectrum of intracranial aneurysms, a balance of prospective data and clinical experience is necessary to properly and individually assess an individual patient’s rupture risk.

Of those patients who experience (SAH) after aneurysmal rupture, approximately one third return to a functional life, one third live a dependent life, and the last third do not survive.^1,5,7,9 As advances in neurocritical care have increased survivability, neurological morbidity rate remains about the same. The greatest risk after the initial aneurysmal rupture is for re-rupture. Once the aneurysm is secure, the greatest risk is of cerebral vasospasm and ischemic complications from such events, thereby underlying the importance of early intervention and close monitoring in the postrupture period.

Pathogenesis

Intracranial arteries are unique to the systemic vascular system in that they lack the external elastic lamina present in extracranial vessels (Fig. 13.1). The pathogenesis of intracranial aneurysms has been thought to be due to a number of congenital factors such as vascular wall defects (i.e., media and elastic lamina), hemodynamic load on tortuous segments and bends with or without branch formation in the appropriate distribution, and discontinuity of the tunica media at origins of small vessels from larger parent vessels. Certainly, a multitude of systemic factors are thought to contribute to aneurysmal pathogenesis, such as degenerative changes, hypertension, atherosclerosis, connective tissue disease, and hemodynamic stress.

FIGURE 13.1 Histological layers of cerebral arteries. Note the absence of media in the aneurysmal wall and the fragmented internal elastic lamina. The wall may be quite sclerotic in some areas and extremely thin in others.

Genetic predisposition through various systemic and syndromic conditions has also been associated with the presence of intracranial aneurysms and is thought to represent approximately 10% to 12% of all aneurysms. Autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, Marfan syndrome, tuberous sclerosis, and fibromuscular dysplasia have all been associated with the presence of intracranial aneurysms.^10–15 In recent years, many genetic loci have been proposed to be associated with familial linkage. Ruigrok and associates¹⁴ recently reviewed the genetics of intracranial aneurysms and reported that probable loci included chromosomes 5q and 17cen, from which the strongest associations code for versican, an extracellular matrix protein, and TNFRSF13B, a transmembrane activator and a calcium modulator ligand interactor, respectively. Other suggestive loci are 1p34.3-p36.13, 7q11, 19q13.3, and Xp22.^9,14,16,17

Despite the numerous factors likely to be related to intracranial aneurysm pathogenesis, it is most likely a complex, multifactorial set of circumstances involving anatomical, environmental, and genetic factors that lead to arterial wall weakening and aneurysm formation (Fig. 13.2). In fact, multiple aneurysms are present in up to 30% of patients. However, the majority of lesions are located at branching points along the proximal arterial tree, suggesting that hemodynamic factors play a significant role in aneurysm formation. In addition, formation of de novo aneurysms has been shown to occur at communicating arteries, and fatal rupture of aneurysms has occurred after recruitment of collateral blood flow through communicating arteries after the occlusion of carotid arteries. Furthermore, the incidence of aneurysms associated with high-flow states (e.g., arteriovenous malformations) is higher than in the general population, and some of these lesions regress after treatment of the vascular malformation. Finally, recurrent aneurysms can develop after incomplete treatment, whether by endovascular or microsurgical means.

FIGURE 13.2 When high-flow situations complicate cerebral hemodynamics, such as an intracranial arteriovenous malformation, aneurysms are found with a relatively high frequency on feeding arteries and often in atypical distal sites.

Other factors related to aneurysm formation are trauma, infection, and tumor emboli. Traumatic aneurysms are more often fusiform and located near the skull base. Infectious aneurysms have a multitude of etiological factors but most commonly occur secondary to bacterial endocarditis. Finally, tumorigenic aneurysms are thought to form as a result of seeding of the arterial wall through hematogenous spread and are most often related to cardiac myxomas.

Natural History

The natural history of intracranial aneurysms can be conceptually separated into two general areas, namely, ruptured and unruptured. Of those patients who experience aneurysmal SAH, approximately one third will not survive 2 weeks after hemorrhage, one third will survive but have a dependent existence, and the last third will survive and be fully independent. The peak risk of re-hemorrhage is within the first 24 to 48 hours, with a 4% re-rupture risk within the first 24 hours, and 30% of patients rebleeding within 2 weeks if not treated.

For patients with unruptured intracranial aneurysms, the natural history is much more difficult to resolve. Prior to 1998, the estimated rupture rate for aneurysms was thought to be 1% to 2.5% per year cumulatively. For young patients, the data suggested that intracranial aneurysms should be treated, as the cumulative risk of rupture over many years is very significant. However, the largest and most debated prospective database on unruptured intracranial aneurysms was published in two parts by the International Study of Unruptured Intracranial Aneurysms (ISUIA) and suggested that the rupture risk of unruptured asymptomatic aneurysms was much more benign than once thought (see Table 13.1). The 5-year cumulative rupture rate without a prior history of SAH of anterior circulation aneurysms (not including cavernous carotid or posterior communicating artery aneurysms) was 0%, 2.6%, and 14.5% for aneurysms less than 7 mm, 7 to 12 mm, and 13 to 24 mm, respectively, and it was 2.5%, 14.5%, and 18.4%, respectively, for the same three size groups of aneurysms in the posterior circulation (including posterior communicating artery aneurysms). Patients with a history of SAH with aneurysms less than 7 mm had a 1.5% rupture rate over 5 years with further increases in rates with increasing aneurysmal size. Many limitations of the ISUIA study have been reported. Selection bias likely played a substantial role because patients with aneurysms that were thought to be at a high risk of rupture, namely, those with multiple lobulations, hemodynamic factors, and so on, were treated and therefore were not included as part of the study. Further, cavernous carotid aneurysms were included in these studies, but these aneurysmal lesions rarely result in SAH. Lastly, the annual incidence of SAH in the United States is approximately 30,000, which when calculated against the incidence of aneurysms, results in a rupture rate of at least 1% per year, significantly higher than that calculated in the ISUIA study.^18,19

Other morphological factors of aneurysms, besides the size of the aneurysmal dome, have been thought to contribute to the annual rupture risk. More specifically, neck width, dome width, aneurysm shape, aspect ratio (height/neck width), and bottleneck factor (dome width/neck width) have been examined.⁸ Among these, a higher aspect ratio (>1.6) is thought to be associated with an increased rupture risk. Other morphological characteristics, such as lobulations, daughter sacs, and surface irregularity, have long been associated with higher rupture risk⁸ (Box 13.1). Finally, the hemodynamics of the surrounding vasculature to an unruptured aneurysm may put a particular lesion at a greater risk of rupture, for example, dominant A1 feeding into an anterior communicating artery aneurysm.²⁰

Clinical Presentation

The clinical presentation of patients who harbor intracranial aneurysms can be divided into several categories, namely, incidental (asymptomatic or unrelated symptoms), cranial nerve and other neurological deficits, sentinel events, or frank rupture (SAH).

For patients who present with frank aneurysm rupture, the most common clinical symptoms and signs are the sudden onset of the worst headache of their life, severe nausea and vomiting, altered mental status, nuchal rigidity, and loss of consciousness. Most emergency departments automatically order a head computed tomography (CT) scan without contrast to evaluate these patients for possible SAH, although misdiagnosis remains a major problem (Fig. 13.3). It is of paramount importance to identify these patients because aneurysmal re-rupture has devastating consequences. With the technological advancements of CT scanners, the sensitivity/specificity of SAH detection is greater than 98% in the first 2 days.²¹ As such, lumbar puncture is not necessarily indicated unless the insinuating event happened at least 3 days prior or if head CT image is negative despite strong clinical suspicion. A lumbar puncture is used to detect evidence of red blood cells and xanthochromia. After confirmation of SAH on CT scan, a CT angiogram (CTA) is performed, especially if the clinical history is highly suggestive of aneurymal SAH. CTA detection of intracranial aneurysms is now on the order of 99% for aneurysms larger than 2 mm.^22,23 Digital subtraction angiography (DSA) is now often reserved at our center for the absence of or questionable intracranial lesions seen on CTA or when the clinical picture favors endovascular intervention.

FIGURE 13.3 Noncontrasted computed tomography (CT) scan of the head showing diffuse subarachnoid hemorrhage (SAH) with mild enlargement of the ventricular temporal horns.

Approximately 25% of patients who present with SAH have had sentinel headaches (same symptoms as those related to SAH) in the weeks prior to presentation. The diagnosis of “sentinel headache” is only made in retrospect if the patient did not seek medical attention or was misdiagnosed recently when evaluated. These “sentinel headaches” are thought to be due to “minor leaks” or acute aneurysm expansion. Education of both the public and the medical community (especially physicians from primary care, neurology and emergency medicine) could go a long way to earlier diagnosis and improvement of outcomes. Any sudden onset thunderclap headache should be assumed related to an intracranial aneurysm until proved otherwise.

Various neurological deficits can be detected in aneurysm patients due to local mass effect, increased intracranial pressure, or thromboembolic complications from progressive thrombosis of a large or giant aneurysm. Common neurological findings include third cranial nerve palsy, visual loss (afferent pupillary defect), trigeminal symptoms, sixth cranial nerve palsy, nystagmus, vertigo, persistent nausea, and altered mental status (Fig. 13.4). These symptoms can occur from progressive enlargement of an unruptured aneurysm (Fig. 13.5). Focal neurological deficits can occur with embolization of clot from a thrombotic aneurysm. Magnetic resonance imaging (MRI) may be indicated in the workup of neurological findings but should not overlook the possibility of either aneurysms or the presence of subarachnoid blood.

FIGURE 13.4 A patient with a third cranial nerve palsy will exhibit some or all of the following signs: ptosis, pupillary dilation, and inability to elevate, depress, or medially deviate (adduct) the eye. These findings (particularly pupillary dilation) strongly suggest focal mass effect.

FIGURE 13.5 The potential evolution of a small aneurysm into a large and finally giant aneurysm. With each stage of enlargement, the efferent branches migrate farther out onto the sac itself.

Once aneurysmal SAH has been confirmed, the initial neurological examination is important in determining prognosis. A variety of grading scales have been developed, most commonly the World Federation of Neurosurgical Societies (WFNS) and Hunt-Hess grading scales (Table 13.2). Morbidity and mortality rates increase with a higher grade in each scale.

Initial treatment for SAH involves a complete medical evaluation. Some patients can present with acute mental status changes that are the result of hydrocephalus. In these cases, an extraventricular drain should be placed not only to relieve the hydrocephalus but also to monitor the intracranial pressure. Permanent cerebrospinal fluid (CSF) diversion is necessary in approximately 10% of patients, owing to the hematoma breakdown products affecting the functioning of the arachnoid granulations. However, the most common medical complication after SAH is cerebral ischemia secondary to cerebral vasospasm. Vasospasm usually starts by the fifth posthemorrhage day and can be a threat for up to 14 days after hemorrhage. Angiographic vasospasm has been shown in up to 70% of patients, whereas symptomatic clinical vasospasm occurs in only about 30% of patients.^24–26 Medications often administered to SAH patients, namely nimodipine, a calcium channel blocker, and pravachol, an HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitor, are thought to limit, although not prevent, the onset of symptomatic vasospasm, thereby improving outcomes, not incidence.²⁷ However, controversy still exists regarding the absolute effects of these medications.

Subarachnoid Hemorrhage

Treatment of Subarachnoid Hemorrhage

Modern evaluation and treatment of intracranial aneurysms requires the participation of a multidisciplinary team, including neurosurgeons, neuroradiologists, endovascular practitioners, and neurocritical care specialists. Each patient has to be considered on an individual basis and the strategy for treatment is unique to each patient. In the current era, the options for treatment of intracranial aneurysms are observational, endovascular, microsurgical, or a combination of approaches.

The goal of treatment is to exclude the aneurysm from the circulation with minimal morbidity to the patient. Because the peak incidence of re-hemorrhage for ruptured aneurysms occurs within the first 48 hours, the most effective strategy to minimize this risk is to secure the ruptured aneurysm as soon as possible. However, if a patient presents at “off hours,” the risks presented by suboptimal operating room and staff conditions may outweigh the risks of doing the procedure in the acute phase. It is therefore recommended to perform aneurysm surgery on the next elective surgical day, when an appropriate neurosurgical team can be assembled. Furthermore, each ruptured aneurysm is unique and may present technical challenges that may make surgery difficult, thereby necessitating endovascular therapy in the acute phase. However, a ruptured aneurysm should be secured before the onset of delayed cerebral ischemia so as to avoid the risk of re-hemorrhage with potential hypertensive and hypervolemic therapy for vasospasm. Despite this rationale, the issue of treatment timing remains somewhat controversial.

Systemic circumstances (e.g., cardiopulmonary instability) may prevent a patient from being ready for aneurysm treatment. Therefore, antifibrinolytic therapy has been suggested to aid in reducing the risk of re-bleeding. The Cooperative Aneurysm Study found that the re-bleeding rate at 14 days was 11.7% if antifibrinolytics were used and 19.4% if no antifibrinolytics were used.³⁷ However, in the face of vasospasm, the risk of ischemic events is higher in patients in whom antifibrinolytics were used, thus equalizing the mortality rates between the two groups. As such, we tend to use antifibrinolytics in patients who present in poor grade or who are medically unstable for treatment with the knowledge that ischemic complications are possible and CSF diversion may be necessary.

Symptomatic vasospasm is the leading cause of morbidity and death following aneurysmal SAH.^25,26 Treatment for vasospasm has evolved over the past decade but still lacks definitive treatment (Fig. 13.6). Patients require diligent monitoring and treatment for up to 14 days after hemorrhage through invasive blood pressure monitoring, cerebral blood flow monitoring (transcranial ultrasound, CT/MRI perfusion studies), and often aggressive medical therapy including hypertensive and hypervolemic therapy and hemodilution (triple H therapy). In symptomatic patients, endovascular therapy can also be employed, which may involve intra-arterial injection of vasodilators or balloon angioplasty. In addition to spasm in the large conducting vessels, the phenomenon of SAH also triggers more complex events, which can lead to patchy infarcts in areas apparently unaffected by angiographically visible vasospasm.

FIGURE 13.6 Prophylactic and therapeutic strategy for vasopasm at Northwestern University Medical School.

Much study has been invested in pharmacological prevention of arterial narrowing but research has not demonstrated changes in the long-term outcome of patients treated with such agents. Calcium channel blockers (e.g., nimodipine) have been used since the 1980s but have produced modest results in the literature.^38–41 More specific pharmacological agents, namely, selective endothelin 1a receptor antagonists, have shown promise in effectively preventing and reducing arterial narrowing but failed to demonstrate any effect in long-term outcomes.^25,26 Lastly, it has been suggested that statin therapy in conjunction with calcium channel blockers may lower the incidence of delayed cerebral ischemic events and improve patient outcomes; this was demonstrated in a phase II study.⁴² However, a recent meta-analysis of the literature claims that no statistical benefit could be gleaned from the literature. Nevertheless, many institutions now initiate acute therapy with both calcium channel blockers and statins.⁴³

Approximately 70% of patients demonstrated some form of radiographic arterial narrowing, which does not necessarily warrant immediate treatment. However, up to 30% of these individuals will progress to have clinically symptomatic vasospasm, warranting immediate evaluation and treatment, medical or otherwise. Monitoring vasospasm in comatose patients becomes problematic because of the absence of a clinical examination to follow, thereby placing emphasis on indirect evidence such as transcranial Doppler or CT/MRI perfusion studies on progressively worsening cerebral blood flow changes to indicate time of potential treatment. Medical management of vasospasm has traditionally been through “triple H” therapy, involving hemodilution, hypertension, and hypervolemia.^26,30,38,41 Maximizing the rheological properties of blood (i.e., maintaining a hematocrit level from 30 to 34) improves tissue perfusion. Should a focal neurological deficit develop, we immediately raise the systolic blood pressure up to the 175 to 200 mm Hg range or until the deficit reverses. In addition, we will volume expand and raise the central venous pressure (CVP) of the patient to the 10 to 15 mm Hg range. If these medical maneuvers do not result in an improvement of the patient’s condition and a surveillance CT scan does not demonstrate any areas of obvious infarction, we then proceed immediately to the angiography suite for a diagnostic angiogram and potential intra-arterial therapy.

Hydrocephalus, either communicating or noncommunicating, frequently develops in the first few days after SAH and partly explains the appearance of a globally edematous brain. Upon recognition that symptomatic hydrocephalus exists, it is suggested that CSF diversion be performed, usually by placement of an extraventricular drain (EVD). Careful placement of an EVD and conservative drainage of CSF must be maintained to avoid the possibility of an acute increase in the transmural pressure across the aneurysm or ventricular shift leading to the destabilization of the tamponading aneurysmal clot. In about 10% of patients, permanent CSF diversion is necessary.⁴⁴ The risk of permanent hydrocephalus is higher in patients with ruptured upper basilar trunk aneurysms.

Treatment of Intracranial Aneurysms

The treatment of intracranial aneurysms has undergone a paradigm shift such that endovascular therapy has emerged as a viable treatment regiment and is first-line therapy in several European countries. Aneurysm treatment in the United States is less standardized with both microsurgical and endovascular strategies employed depending on the individual lesion and surgeon/patient preference. However, endovascular therapy of intracranial aneurysms will not be discussed here as it is discussed elsewhere in this textbook. We will focus on the general problems caused by aneurysms in various locations such as anterior circulation artery aneurysm, proximal and posterior carotid artery wall aneurysm, caritid bifurcation, middle crerbral artery bifurcation, anterior communicating artery, distal basilar artery, vertebral artery and posterior inferior cerebellar artery, vertebral confluence, and lower basilar trunk, and illustrate the anatomical complexities and unique features found by neurosurgeons treating these various lesions. New developments over the past several years include advanced microscopic technology, intraoperative imaging techniques, neuromonitoring, and pharmacological agents utilized to aid clip reconstruction of complex aneurysms.

Adjunctive Techniques in Aneurysm Surgery

Several advancements have been made in adjunctive techniques and equipment that have significantly improved the surgical evaluation and management of aneurysms. Although the surgical microscope has been utilized in surgery for decades, its impact on aneurysm surgery continues to improve. With the reduction in the size of the microscope head as well as improvement in optics, neurosurgeons can work more comfortably and with improved visualization. The addition of using intraoperative fluorescence techniques such indocyanine green (ICG) video angiography allows the evaluation of aneurysm clip reconstruction in a fast and safe manner without the added risks of intraoperative catheter angiography.^45–47 This imaging modality can be repeated multiple times during the procedure. Although catheter angiography remains the gold standard of intracranial vascular imaging, this new modality of intraoperative imaging allows quick and repeated evaluation of aneurysm clipping. Pharmacological agents have also been used more recently to aid in the clipping of complex intracranial aneurysms. Adenosine-induced cardiac arrest provides a safe method to reduce cerebral blood flow and softening of the aneurysmal dome, allowing manipulation and improved clip placement and reconstruction.^48–50 With adequate cerebral protection, adenosine obviates the need for temporary clip occlusion in carefully selected cases. However, in most cases, patients can tolerate temporary occlusion without issue (Fig. 13.7). These measures are only a few of the recent and important developments to aid in aneurysm surgery. With the ever-advancing technology of intraoperative navigation and imaging, aneurysm surgery will become safer and more efficient.

FIGURE 13.7 A to C, Temporary arterial occlusion is often necessary in repairing complex large or giant aneurysms. Not infrequently, the aneurysm must be widely opened to allow evacuation of debris and thrombus before definitive clip reconstruction can be performed.

Surgical Management of Anterior Circulation Artery Aneurysms

Pterional “Frontotemporal” Craniotomy

The pterional craniotomy has been the workhorse surgical approach for a variety of anterior circulation artery aneurysms because of its versatility and many modifications. A key element of this approach is the patient’s head position. Careful attention to this basic first step facilitates exposure and allows complex procedures to be carried out through small, tailored craniotomies, limited dural openings, and often without the need of brain retractors. The most frequent means of skull fixation in aneurysm surgery is the Mayfield-Keys three-point device, which provides almost absolute head stability (Fig. 13.8). Positioning of the three points varies for a pterional craniotomy and is at the discretion of the operating surgeon. Once the head is secured in the fixation device, the neurosurgeon performs three distinct maneuvers to position the head optimally for the necessary intracranial exposure.⁵¹

FIGURE 13.8 The Mayfield-Keys three-point skull fixation device provides optimal head stability so that inadvertent patient movement will not result in catastrophic injury to neural or vascular structures.

Rotation of the head is the first maneuver and is usually toward the contralateral or nonoperated side to an angle determined by the target anastomotic site (Fig. 13.9A). When the target site is the internal carotid or the distal basilar artery, minimal head rotation is required, usually approximately 20 degrees. Further angulation will allow the temporal lobe to migrate via gravity posteriorly and medially into the incisura and thus potentially obstructing the operative window. Aneurysms of the middle cerebral artery bifurcation require more angulation, approximately 40 to 45 degrees, to expose the sylvian fissure maximally, allowing both the temporal and frontal lobes to fall posteriorly once released from the fissure. For aneurysms of the anterior communicating artery, even more rotation is needed, approximately 45 to 60 degrees, to simplify the exposure of the medial gyrus rectus and interhemispheric fissure.

FIGURE 13.9 Patient positioning for pterional craniotomy. A, Rotation. The head is elevated slightly relative to the thorax and rotated contralaterally by an extent dictated by the specific operative target (less rotation for carotid and basilar bifurcation aneurysms and more rotation for aneurysm of the middle cerebral artery or anterior communicating region). B, Flexion. The neck should then be gently flexed, bringing the chin toward the contralateral clavicle. This subtle maneuver orients the floor of the anterior cranial fossa perpendicular to the long axis of the patient’s body, maximizing the surgeon’s access to the anatomical target without encroachment on the patient’s ipsilateral shoulder. C, Extension (tilt). While maintaining the previous elements of rotation and flexion, the vertex is tilted inferiorly so that the maxillary eminence rises superior to the brow. The degree of extension will vary somewhat with the target aneurysm (less for paraclinoidal aneurysms and more with distal basilar aneurysms).

Flexion of the head is designed to maintain a perpendicular relationship between the floor of the anterior cranial fossa and the long axis of the patient’s body (Fig. 13.9B). After positioning the head in the appropriate rotation, the neck is flexed gently, bringing the chin toward the contralateral clavicle without compromising cervical venous return. This maneuver brings the area of operation away from the ipsilateral shoulder.

Extension or “tilting” of the head allows the frontal lobe to fall away from the floor of the anterior cranial fossa (Fig. 13.9C). To minimize retraction of the brain and to optimally display the vascular structures at the skull base, the vertex of the skull is tilted inferiorly so the maxillary eminence rises superior to the brow ridge.

Surgical Technique

The surgical incision is first drawn on the skin beginning at the level of the zygoma, 1 cm anterior to the tragus, and extends superiorly immediately behind the hairline and gently curves anteriorly to the midline (Fig. 13.10). A simple technique is to put the thenar eminence of the hand onto the brow ridge and rotate the hand starting at the zygoma. A curvilinear marking will result that just approaches the midline. Every attempt is made to keep the incision behind the hairline for cosmesis, although this can be difficult in a balding patient. Numerous options are available for reflecting the scalp. The most common scalp flap is the myocutaneous flap, which involves reflecting the scalp and temporalis muscle together anteriorly (Fig. 13.11). An alternative technique involves the interfacial dissection where the bulk of the temporalis muscle is reflected inferiorly and the intrafascial fat pad, containing the frontalis branch of the facial nerve, and the scalp are reflected anteriorly. When reflecting the scalp and temporalis muscle, the key target of exposure with respect to the skull is the anatomical keyhole. A variable amount of temporal squama is exposed as well, depending on the vascular target. Bur hole placement normally consists of one bur hole in the anatomical key, one at the floor of the middle fossa, and one just inferior to the superior temporal line posteriorly (Fig. 13.12). There are some aneurysmal lesions (e.g., carotid wall, anterior communicating, and basilar apex aneurysms) that may require additional bony removal in addition to the standard pterional craniotomy. The addition of an orbital or orbitozygomatic (OZ) osteotomy may add 10 to 15 degrees of exposure, which is especially helpful in situations in which a swollen, tense brain exists (Fig. 13.13). To prepare for the additional craniotomy, the dura overlying the orbital roof is stripped posteriorly toward the orbital apex, medial to the cribriform, and lateral to the dura of the superior orbital fissure. If exposed, the periorbita is stripped from the superior and lateral walls of the orbit to a depth of approximately 3 cm. If the zygomatic process is to be included in the osteotomy, the full extent of the zygomatic arch is exposed prior to the reflexion of the temporalis muscle. Resection of the orbital zygomatic segment is best accomplished with a combination of reciprocating saw and osteotomes. The initial bone cuts are made with a reciprocating saw through the supraorbital ridge and frontal zygomatic process with the former being just lateral to the supraorbital foramen. Narrow osteotomes complete the resection across the orbital roof and the greater and lesser wings of the sphenoid bone. Once the masseter has been released from the inferior surface of the zygomatic arch, the piece may be removed en bloc. It is important to preserve at least 3 cm of the orbital roof and lateral wall so as to minimize the possibility of a postoperative pulsatile enophthalmos.

FIGURE 13.10 The skin incision for the pterional craniotomy extends from the zygoma to the midline, curving gently just posterior to the hairline.

FIGURE 13.11 A commonly employed means of opening the scalp involves incision of the skin, galea, temporalis fascia, and muscle with reflection of the resultant flap in a single layer.

FIGURE 13.12 The pterional craniotomy is performed with power instruments so that three bur holes are placed: one at the anatomical key, one inferiorly on the temporal squama, and one posteriorly just inferior to the superior temporal line. The bone is cut as shown, exposing the frontal and temporal dura and the sphenoid ridge.

FIGURE 13.13 Demonstration of orbital (A) and orbitozygomatic (B) osteotomies.

Perhaps the most important element to the extended pterional is the resection of the proximal lesser and greater wings of the sphenoid bone inclusive of the anterior clinoid process. This bony resection is particularly useful for ophthalmic and superior hypophyseal aneurysms. The postclipping reconstruction is performed in a standard fashion with a microplating system and a hydroxyapatite compound or methylmethacrylate to fill in any bony defects.

Depending on the adherence of the dura or in older patients, a fourth bur hole may be placed in the frontal bone just superior to the midline of the superior temporal line. It is important to try to separate the dura from the bone flap through the bur holes with a Penfield 2 or 3. This maneuver will allow easier removal of the bone flap. A craniotome is used to make cuts between the bur holes. After the bone flap is removed, the anterior temporal bone is extracted with rongeurs, as is the lateral third of the sphenoid ridge. Often it is necessary to remove the deepest portion of the sphenoid ridge with a power drill (Fig. 13.14). The inner table of the frontal bone is also removed with careful drilling. This maneuver allows exposure of the parasellar region with minimal frontal retraction. The dural opening is centralized around the sylvian fissure and has a semilunar shape (Fig. 13.15).

FIGURE 13.14 After removal of the bone flap, the sphenoid ridge is resected to the level of the orbitomeningeal artery. The inner table of the frontal bone can also be resected. This maneuver is particularly useful in exposing the anterior communicating region.

FIGURE 13.15 The dura is opened in a semilunar fashion and reflected with stay sutures.

After the surgical microscope is sterilely draped, it is positioned into place so that the parasylvian region can be easily visualized. Following the sphenoid ridge along the inferior frontal lobe will lead to the carotid cistern where the optic nerve and the carotid artery should be easily visualized. The surrounding arachnoid membranes, including the medial sylvian fissure, are opened sharply to separate the medial frontal and temporal lobes from the underlying carotid cisternal structures (Fig. 13.16). After this maneuver, the entire subarachnoid course of the carotid artery, including the bifurcation into the middle and anterior cerebral arteries, should be seen. From this point, the specific aneurysmal site governs the principles of further dissection.

FIGURE 13.16 Sharp microinstruments are used to fully dissect the parasellar cisterns from the prechiasmatic cistern across the carotid cistern into the medial aspect of the sylvian fissure.

Aneurysms of the Proximal (Paraclinoidal) and Posterior Carotid Artery Wall

This unique group of aneurysms arises from the most proximal intracranial segment of the internal carotid artery. Most of the aneurysms in this area can be separated into three subgroups, namely, carotid-ophthalmic, superior hypophyseal, and proximal posterior carotid wall. Each of these aneurysms presents several unique technical problems to the neurosurgeon. Although their proximity to the skull base was once a formidable problem in regard to obtaining any significant proximal vascular control, endovascular access and proximal control have reduced this difficulty. When these aneurysms reach a significant size, they can compress and distort the optic nerve, resulting in visual neurological deficits. The aneurysm must then be decompressed to relieve the mass effect. Further, large and giant aneurysms are often found to have thick, calcified walls, which must be refashioned with creativity, requiring multiple aneurysm clips because of the rigidity and differential wall thickness. The lateral aspect of paraclinoidal, especially carotid-ophthalmic, aneurysms can be partially covered by the anterior clinoid process as it emerges from the roof of the cavernous sinus (Fig. 13.17). The optic strut, the inferior bony aspect of the optic canal, can also obscure the proximal neck of the aneurysm. Our experience suggests that although large aneurysm domes can distort various neurovascular structures, the proximal portion of the normal carotid artery is always located at the lateral aspect of the optic canal. As such, this proximal portion of the carotid can normally be exposed via an incision in the falciform ligament, which will uncover the proximal carotid and ophthalmic artery origin, and the proximal neck of the aneurysm, particularly in carotid ophthalmic and superior hypophyseal variants. If the aneurysm projects laterally or arises from within the carotid cave, then aggressive bony resection of the anterior clinoid process or the optic strut will be required to demonstrate the proximal neck. In ruptured proximal carotid aneurysms, it is important for proximal control to be established early either through an open cervical exposure to the internal carotid artery or through endovascular means with a proximal internal carotid balloon. Either way, it is important to guarantee early proximal control should difficulties arise and require temporary arterial occlusion, aneurysm decompression, and intraoperative angiography.

FIGURE 13.17 Proximal carotid (paraclinoidal) aneurysm. A, These aneurysms often distort and attenuate the optic nerve and may have their proximal neck obscured by the dura covering the lateral aspect of the optic canal or by the bony anterior clinoidal process. Without securing proximal control in the neck or by endovascular means, it is obvious that true control of this aneurysm may be achieved intracranially only at some peril. B, To resect the anterior clinoid process, a dural flap is fashioned and reflected over the fundus of the aneurysm. A high-speed drill is then used to remove as much bone as is necessary to expose the proximal neck of the aneurysm. C, The specific clip placement chosen must not jeopardize the optic nerve or the patency of the internal carotid or the ophthalmic artery.

Posterior carotid wall aneurysms include lesions arising immediately distal to the posterior communicating artery as well as those arising immediately distal to the origin of the anterior choroidal artery (Fig. 13.18). These lesions are some of the most common aneurysmal lesions seen in neurosurgical practice, and intimate knowledge of the microanatomy is paramount in order to treat these lesions successfully. Neurological signs of an enlarging aneurysm in this area are pain, from compression of the tentorial incisura, and third cranial nerve deficits. The intimate association between the distal neck of the internal carotid–posterior communicating artery aneurysm to the fragile anterior choroidal artery place it at risk when treating these aneurysms. Injuring the anterior choroidal artery, which supplies the posterior limb of the internal capsule, the lentiform nucleus, the optic tract, the amygdala, and the choroid plexus of the temporal horn, can result in profound and devastating neurological deficits, including hemiplegia and hemianopia. Maneuvers that can result in injury include aggressive dissection of the aneurysm dome and the placement of Gelfoam or cotton to control minor intraoperative bleeding. It should be emphasized that the distal course of the anterior choroidal artery often runs close to the aneurysmal dome and should be carefully dissected away so that the distal clip blade does not compromise its blood flow or the vessel becomes “accordianed” by clip closure (Fig. 13.19). The posterior communicating artery usually arises just proximal to the aneurysmal neck, and every attempt should be made to preserve this vessel because of important anterior thalamoperforating branches that ramify from its proximal portion. The neurosurgeon should also know if the posterior communicating artery is of fetal origin, therefore lacking an ipsilateral P1 segment. In this situation, it is paramount to not sacrifice this artery. However, in patients with a normal circle of Willis, it is sometimes acceptable to include the posterior communicating artery in the clip, assuming the anterior thalamoperforators will fill from retrograde flow from the P1 segment off the basilar artery. This maneuver should be reserved for extreme situations because we have seen major deficits arise from it. Nevertheless, when possible, all components of the circle of Willis should be preserved, particularly in the setting of potential vasospasm after SAH and reliance on available collateral pathways. The most common clip arrangement for a posterior communicating artery aneurysm is perpendicular to the carotid artery. In smaller aneurysms, the carotid artery may narrow a bit after clipping but is usually trivial. In larger broad-based aneurysms, clipping perpendicular to the carotid artery can substantially narrow, even wrinkle, the carotid artery and impose shear forces on the fragile neck of the aneurysm during the closure of the clip. The angled fenestrated aneurysm clip allows clip placement so that the blades close parallel to the carotid artery, minimizing the shear forces. Regardless of the clip chosen, it is critical to inspect the course of the anterior choroidal and the posterior communicating arteries to ensure that these vessels have not been compromised.

FIGURE 13.18 Posterior carotid wall aneurysm. Despite their frequency and relative simplicity, especially the ease of achieving early proximal control intracranially, the neurosurgeon should not be nonchalant or complacent. The anterior choroidal artery is in intimate relationship with the distal neck, and simple retraction and mild compression can have devastating consequences.

FIGURE 13.19 Alternatives for clipping posterior carotid wall aneurysms. A, For small aneurysms, a direct clip placement perpendicular to the carotid artery is often the best alternative. B, For larger aneurysms in this location, the degree of “gathering” of tissue by a perpendicular clip placement can jeopardize the carotid artery as well as apply serious shear stresses to the aneurysm neck during closure. The aperture clip allows blade closure parallel to the carotid artery, minimizing these deleterious events.

For patients presenting with third cranial nerve deficits, the aneurysm dome is not dissected away from the nerve. This maneuver can further damage the cranial nerve. Instead, the aneurysm is evacuated of its contents after clipping to eliminate the direct pulsations by the aneurysm on the nerve. Simple decompression will result in restoration of function in most patients within 6 months.

Aneurysms of the Carotid Bifurcation

Despite the fact that the carotid terminus/bifurcation is subject to continuous hemodynamic stress, it is a relatively rare site for aneurysm development. Aneurysms in this location typically project superiorly and occasionally superoposteriorly. Rupture of these aneurysms can often result in an intraparenchymal hematoma that mimics that of a putaminal hypertensive hemorrhage with little to no true subarachnoid blood. The diagnosis of aneurysmal rupture in these patients, especially without a history of hypertension, can be difficult.

Appropriate operative exposure of the carotid terminus/bifurcation requires judicious drilling of the sphenoid ridge and dissection of the opercular-insular cortex as well as the sphenoidal portions of the sylvian fissure. We prefer a lateral to medial approach followed by dissection of the carotid cistern to allow “unfolding” of the anatomy at the carotid terminus. The aneurysmal dome and neck can often be intimately associated with local vascular structures, namely, the anterior choroidal artery, anterior cerebral artery, the recurrent artery of Heubner, and sometimes medial lenticulostriate branches from the middle cerebral artery (Fig. 13.20). These vessels typically hide posterior to the aneurysmal dome. It is paramount that the operating surgeon identify all of these important vessels so that the clip blades do not include them during closure of the aneurysm clip.

FIGURE 13.20 Aneurysms of the internal carotid artery bifurcation are frequently in intimate association with the distal course of the anterior choroidal artery as well as the medial lenticulostriate arteries arising from the middle and anterior cerebral arteries.

The two most important aspects of the exposure are gaining proximal control of the internal carotid artery and a wide opening of the carotid cistern. In addition, the sylvian fissure should be opened completely to expose the M1 segment, which can be followed proximally to the carotid terminus/bifurcation. Full exposure of the carotid terminus/bifurcation ensures both afferent and efferent circulation control. When treating difficult large and giant carotid terminus aneurysms, it is paramount for the neurosurgeon to know if there is a patent anterior communicating artery, which, if present, allows the potential sacrifice of the ipsilateral A1 segment in these cases and in the event of tears involving the medial aspect of the aneurysmal neck (Fig. 13.21).

FIGURE 13.21 Carotid bifurcation aneurysm. If the anterior communicating artery is known to be patent, a valuable option for ceasing untimely intraoperative rupture is to incorporate the ipsilateral A1 segment into the definitive clipping, thus relying on the contralateral carotid to irrigate the anterior cerebral artery territory bilaterally.

Aneurysms of the Middle Cerebral Artery Bifurcation

Aneurysms of the middle cerebral artery, in particular at the site of the bifurcation, are quite common and hemorrhage from these lesions can produce several unique features. As such, diagnosis can be difficult in terms of the etiology of either an intraparenchymal or subdural hemorrhage in this location. Aneurysms at this location can also become very large or giant due to growth into the substance of the temporal lobe or invagination into the pia-arachnoid of the medial temporal lobe. When rupture occurs at the distal aspect of the aneurysmal dome, the resultant hematoma is in the temporal lobe parenchyma. Patients can present after a middle cerebral artery (MCA) aneurysm rupture with profound mass effect from the hematoma that necessitates surgical evacuation (Fig. 13.22). Modern CT angiography allows the immediate evaluation of the cerebral vasculature in cases such as these so that definitive treatment of the aneurysm can be considered during the evacuation of the hematoma.

FIGURE 13.22 Aneurysms arising from the middle cerebral artery bifurcation often project into the medial aspect of the temporal lobe. Upon rupture, a hematoma may develop primarily within the temporal lobe itself and only minimally involve the subarachnoid space.

The approach to MCA aneurysms is diverse and largely up to the experience and preference of the operating surgeon. One approach is to work medial to lateral from the carotids cistern, identifying the proximal M1 segment through the proximal sylvian fissure and dissecting distally until the bifurcation is reached. The serious disadvantage to this approach is the amount of frontal lobe retraction that is required to adequately expose the proximal M1 segment. Another approach is through the superior temporal gyrus, especially in cases in which there is a temporal hematoma. Finally, the preferred approach to most MCA bifurcation lesions in most institutions is the direct transsylvian approach. The dissection is initiated in the lateral aspect of the sylvian fissure, approximately 2 to 3 cm from the sphenoid ridge. Frequently, an opening in the sylvian fissure can be made in the arachnoid membrane at this point. As the course of the distal sylvian veins is through this fissure, it is important to preserve all of the native vasculature. However, crossing sylvian veins may sometimes be sacrificed in order to open the fissure widely. Dissection via this route allows the surgeon to stay within the subarachnoid space from the outset, minimizing the degree of brain tissue retraction necessary and providing proximal control to be achieved safely. As the dissection deepens within the sylvian fissure, the small middle cerebral branches are followed down to the M2 segments, ultimately leading to the MCA bifurcation and M1 segment. Careful inspection of the aneurysm is important in this area because the M2 segments can often be intimately associated with or incorporated into the aneurysmal neck or dome. Dissection of these vessels must be carefully done to ensure continued distal blood flow after clipping. In cases of large or giant aneurysms that incorporate efferent vessels in the aneurysmal dome, these vessels may be either reimplanted into the distal vasculature or perfused with the aid of a revascularization strategy.

Aneurysms of the Anterior Communicating Artery

Aneurysms of the anterior communicating artery are perhaps the most common cause of SAH and represent approximately 30% of all cases of ruptured intracranial aneurysms. Furthermore, aneurysms in this location are thought to rupture at smaller diameters than those in other locations. The anterior communicating artery as well as the A1 segments of the anterior cerebral artery are some of the most variable components of the circle of Willis. The combination of hemodynamic factors with aberrant anatomy more often explains the propensity of aneurysm development in this location. Common anatomical anomalies are irregularities in size, asymmetrical dominance of A1 segments, and fenestration, duplication, or triplication of the anterior communicating artery. In fact, most anterior communicating artery aneurysms are thought to arise from the junction of the dominant A1 segment and the anterior communicating artery. Hemorrhagic presentation of ruptured aneurysms in this location can be highly varied and include diffuse SAH, interhemispheric SAH, intraventricular hemorrhage (by rupture through the lamina terminalis), and intraparenchymal hemorrhage (usually a flame-shaped frontal lobe hematoma). Unless they reach a large or giant size, aneurysms in this location rarely present with neurological deficits.

Treatment of anterior communicating artery aneurysms can present the surgeon with unique challenges. To adequately expose the surgical target, the bony craniotomy should be carried somewhat more medially and inferiorly than the craniotomy designed for other lesions because of the more anterior location of the anterior communicating artery complex. This is done by enlarging the craniotomy to the midpupillary line and carrying the bony incision as close to the brow as possible, without infiltrating the frontal sinuses. To augment this approach, a significant amount of bone, namely the sphenoid ridge to the superior orbital fissure and the inner tables of the anterior and middle fossa, must be removed. An alternative surgical approach is the fronto-orbito-zygomatic, which involves the lateral superior and lateral orbital wall and zygomatic arch. Both of these approaches can lead to minimal visual obstruction by surrounding bone without significant cosmetic effects.

The microsurgical procedure for anterior communicating artery aneurysms focuses on the wide opening of the carotid cistern. One approach is to locate the proximal portion of the A1 segment at the carotid bifurcation and follow it to the anterior communicating complex. Alternatively, we advocate a direct dissection over the optic nerve toward the midline. The A1 segment swings anteriorly as it approaches the anterior communicating complex. The contralateral A1 segment should then be visualized by crossing the midline and working superior to the contralateral ophthalmic nerve (Fig. 13.23). This cistern may be filled with hematoma if done in a patient with SAH and, therefore, careful dissection in this area should be done to avoid inadvertently injuring the many important vessels traversing this region. The gyrus rectus, just inferior to the olfactory tract, can be aggressively resected with cautery and suction (Fig. 13.24). The overlying veil of pia can be manipulated to facilitate gyral resection. Once the gyrus resection is completed, the ipsilateral and contralateral A2 segments should be identified for distal control. Once both of the A1 and A2 segments are dissected and localized, the dissection can focus on the anterior communicating artery and the associated aneurysm. The relationship of the aneurysm to the surrounding vasculature as well as the proximal and distal aneurysmal necks needs to be understood completely before definite clipping can occur. It is paramount to identify the small perforating arteries that emanate from the posterior aspect of the anterior communicating artery (Fig. 13.25). Laceration or inclusion of these perforators in the clip blades can lead to serious and irreversible cognitive and hypothalamic sequelae.

FIGURE 13.23 Isolation of the contralateral A1 segment completes acquisition of proximal control.

FIGURE 13.24 In approaching anterior communicating artery aneurysms, the additional brain retraction needed to isolate the origin of the A1 anterior cerebral segment at the carotid bifurcation can be avoided by dissecting the gyrus rectus from the optic nerve and tract. Deepening this plane will expose the A1 proximal to the anterior communicating artery.

FIGURE 13.25 Multiple penetrating vessels arise from the posterior aspect of the anterior communicating artery. This schematic illustration shows that the use of excessive clip length and poor visibility behind the aneurysm can cause injury to these important vessels.

Aneurysms of the Distal Basilar Artery

Aneurysms arising from the basilar apex or immediately distal to the origin of the superior cerebellar arteries are the most common form of posterior circulation aneurysms. Access to the distal basilar artery is complicated by the myriad of vital perforating arteries arising from the posterior aspect of the distal basilar artery and both P1 segments (Fig. 13.26). As such, endovascular strategies are often employed as an initial treatment. However, some situations, such as efferent segments off the aneurysmal dome, acute angle of aneurysm neck from parent artery, or failed endovascular therapy make surgery more desirable. To ensure preservation of the vital perforating vessels, clear surgical strategies for clip placement must be made (Fig. 13.27). Pharmacological agents to induce systemic hypotension and asystole (i.e., adenosine) are especially helpful in the narrow surgical corridors through which these aneurysms are treated. Several surgical approaches are used to expose the distal basilar trunk, and the advantages, disadvantages, and limitations are discussed here.

FIGURE 13.26 Aneurysms of the distal basilar artery must be treated with a precise awareness of the constant presence and infinite variability of the posterior thalamoperforating arteries supplying the mesencephalon and diencephalon.

FIGURE 13.27 Clip applied to a basilar bifurcation aneurysm with inadvertent occlusion of thalamoperforating vessels. This error is almost always devastating to the patient.

Pterional Transsylvian Approach

The pterional approach, particularly with wide sylvian fissure dissection, is extremely versatile and used for many aneurysms of the distal basilar complex. Wide dissection of the parasellar cisterns enables access to the interpeduncular cistern by one or multiple routes (Fig. 13.28). The dissection plane and the approach can be developed lateral to the internal carotid artery wherein the posterior communicating artery is followed to the junction of the P1 and P2 segments of the posterior cerebral artery. The P1 can be followed proximally to the basilar artery to gain proximal control. In a similar fashion, a dissection plane can be developed medial to the carotid artery that separates the small perforating arteries to the hypothalamic region and optic tract, opening the membrane of Liliequist, directly exposing the basilar trunk in the interpeduncular cistern. To achieve more superior exposure, the binding arachnoid fibers of the small lenticulostriate vessels can be divided to allow elevation of the optic tract opening up the interpeduncular cistern. To minimize the obstruction of this limited surgical view, the clip applier is often passed lateral to the carotid artery toward the basilar apex. This exposure allows exquisite access to the proximal basilar trunk and both P1 segments for definitive temporary occlusion with aneurysmal decompression, adequate dissection space for large and giant lesions, and, if necessary, control of intraoperative bleeding.

FIGURE 13.28 The surgeon can take advantage of the versatility of the pterional exposure by directing the microscope, and thus the line of sight, medial to the carotid artery and inserting the clip lateral and posterior to the carotid so the bulk of the clip and applier do not obscure the view.

Subtemporal Approach

The lateral view of the interpeduncular cistern offers the ideal view of the vital perforators posterior to the aneurysmal dome (Fig. 13.29). However, visualization of the contralateral P1 segment can be difficult. To improve visualization of the contralateral P1 segment; the space anterior to the aneurysmal neck can usually be gently retracted to expose the initial anterior course of this segment. The initial course of the P1 is superior and anterior. No vessels or neural structures obscure this route. When confusion arises as to whether the identified structure is the P1 or superior cerebellar artery, the P1 is usually white and thicker walled, and if it is followed laterally, the third cranial nerve will be encountered, which clarifies the anatomy. (The P1 is superior to the nerve.) The power of the fenestrated aneurysm clip is especially realized using this approach as the perforating arteries can often be incorporated into the fenestration (Fig. 13.30).

FIGURE 13.29 The subtemporal approach maximizes the surgical view of the thalamoperforating arteries while rendering the access to the contralateral posterior cerebral artery more difficult.

FIGURE 13.30 Aperture or fenestrated clips for subtemporal clipping of basilar bifurcation aneurysms have proved to be immensely valuable. The ipsilateral P1 segment with associated perforating arteries may be safely included in the fenestration.

Extended Lateral Approach

To take the advantages of both the transsylvian and subtemporal surgical approaches, a hybrid approach was developed. The advantage of the transsylvian view is the visualization of all vessels involved in the basilar apex allowing full trapping of the circulation. Unfortunately, this view does not allow adequate visualization of the vital perforators. The advantage of the subtemporal view is visualization of these posterior perforating arteries while the disadvantage is the limited space in which to work, limiting the ability to trap all of the associated vessels.

The extended lateral exposure involves a traditional pterional craniotomy with wide resection of the temporal squama and sphenoid ridge. The sylvian fissure is completely dissected and the sphenoparietal venous drainage is detached from the floor of the middle fossa. With complete sylvian dissection along with gravity, the temporal lobe should migrate posteriorly. The surgical exposure focuses on the third cranial nerve where all of the attachments between the third cranial nerve and the uncus are taken down. A temporal lobe retractor is used to elevate the uncus and all of the temporal lobe structures, which should expose the tentorial incisura as far back as the cerebral peduncle. At this point, full lateral view of the interpeduncular cistern should be realized along with access to all of the vessels for full trapping, if necessary.

Petrosal Approach

The last approach, which consists of a combination of subtemporal, suboccipital, and extended lateral approaches, namely, the petrosal approach, provides the most direct access to aneurysms of the basilar apex to the vertebrobasilar junction. Variations to this approach include a retrolabyrinthine exposure, a partial labyrinthectomy, and a transcochlear resection with facial nerve mobilization. It is the retrolabyrinthine or partial labyrinthine exposure that is most favored at our institution as they are the only petrosal approaches that preserve hearing.

The patient is positioned supine with a shoulder roll ipsilateral to the side of the approach and the head is turned through 90 degrees, then gently extended toward the floor, and, if necessary, the shoulder is taped caudally. A curvilinear incision is made originating 2 cm superior and anterior to the ear and curved along a 2 cm posterior margin from the ear to a point 2 cm inferior to the mastoid tip (Fig. 13.31). The temporalis and occipital frontalis muscles are divided and reflected laterally with the scalp to expose the edge of the external auditory meatus centrally, the temporal zygomatic root rostrally, and the entire mastoid process posterior inferiorly (Fig. 13.32). A mastoidectomy is performed with early identification and skeletonization of the transverse and sigmoid sinuses as far laterally as the jugular bulb. Care is taken to preserve the bony labyrinth in situations in which only a retrolabyrinthine, presigmoid exposure is necessary. With a partial labyrinthectomy, as many as 5 additional millimeters of exposure can be created, providing for several degrees of added maneuverability at the level of the petrous apex. This is accomplished with cautious drilling of the posterior and superior semicircular canals to expose the underlying membranous labyrinth. Once identified, the exposed orifices are immediately waxed off. The horizontal semicircular canal is preserved. A completed mastoidectomy should yield exposure of tegmental and posterior fossa dura. This dural exposure facilitates the addition of a subtemporal and suboccipital craniotomy. The dural opening is typically presigmoid, originating just superior and anterior to the jugular bulb and directed toward the superior petrosal sinus. The sinus is ligated and the dural cut carried rostrally to the dura of the middle fossa, then the dura is tented laterally. The tentorium is coagulated with the bipolar cautery and cut toward the incisura. Care then is exercised to avoid injury to the fourth cranial nerve as it courses adjacent to the midbrain en route to the tentorial edge. The tentorium can be partially excised or coagulated to enhance visualization. The midbrain, clivus, basilar artery, and cranial nerves III to XII are clearly visible with this sigmoid dural exposure with ligation of the nondominant transverse sinus; however, in our experience this maneuver creates an unacceptable risk of venous infarction. We advocate the use of dural grafts and lumbar drainage because watertight dural closures are often very difficult in these cases. We also utilize fat grafts over the dural closure to provide a hydrophobic barrier to leakage and a natural, autologous sealant.

FIGURE 13.31 The typical vertebral-PICA (posterior inferior cerebellar artery) aneurysm is dissected between the fibers of the lower cranial nerves, which exit at the jugular foramen.

FIGURE 13.32 Exposure for mastoid (M), roof of zygoma (Z), and external auditory meatus (E).

Certain surgical nuances improve the surgical treatment of these lesions. If the surgeon avoids the true surgical neck on the operated side and begins the dissection inferior to the P1 origin, the difficultly posed by the broad neck of these aneurysms and the constant finding that the aneurysm dome itself begins to develop well below the superior aspect of the P1 origin can be eliminated. The dissection when performed below the P1 origin allows the surgeon to roll the anatomy out of the interpeduncular cistern and work across the basilar trunk at a site where the distance to be traveled is considerably foreshortened. Once the direction of the posterior thalamoperforators has changed, the contralateral P1 contribution can be visualized. At this point, softening of the aneurysmal dome, whether by pharmacological agents or temporary trapping, a very small fenestrated clip can be placed which incorporates the ipsilateral P1 in the fenestration. The purpose of this clip is to gather the artery neck together and to definitively close the contralateral aspect of the neck. Residual filling through the ipsilateral neck can be closed with a traditional clip across the surgical neck, which gathers the tissue between the P1 origin and the end of the original fenestrated clip.

Aneurysms of the Vertebral and Posterior Inferior Cerebellar Artery

Aneurysms of the intracranial segment of the vertebral artery typically occur immediately distal to the origin of the posterior inferior cerebellar artery (PICA). Hemorrhage is often localized to the lateral aspect of the brainstem and sometimes in the fourth ventricle, through the foramen of Luschka. Aneurysm clipping in this region can be complicated by the intimate relationship between the aneurysm and the cranial nerves emanating from the brainstem, namely, cranial nerves IX, X, XI, and XII.

For surgical exposure, patients are often placed in the lateral position. The body can be held in place via a beanbag or thick tape attached to the bed and patient. Towels should cover the body where the tape is draped over. The legs and the axilla should be padded adequately because these procedures can be lengthy and pressure sores can develop. The dependent arm can be either placed on an armboard or placed in a sling hanging off the head of the bed. The head is flexed and rotated approximately 10 degrees toward the floor. A variety of incisions can be made but those most often used are a curvilinear incision following the posterior aspect of the mastoid down to below the mastoid process or an upside down “U” incision starting at approximately the level of C2 at the midline to the occiput, then over to the mastoid, and then down to the mastoid tip. This scalp flap allows the thick musculature to be reflected laterally away from the craniotomy site. The craniotomy should include the foramen magnum to the ipsilateral condyle and the area just inferior to the junction of the transverse and sigmoid sinuses. After removal, a generous portion of the cerebellar hemisphere is exposed. To minimize cerebellar retraction, a generous amount of CSF can be released by opening the cisterna magna. Once an adequate amount of CSF has been released, the cerebellar tonsil can be gently retracted with a suction device or a dissector to expose the intracranial vertebral artery. The vertebral artery can be followed distally toward the PICA origin, in the process exposing several cranial nerves. Great care is used in dissection as undue trauma to these delicate fibers can result in vocal cord paralysis, swallowing difficulty, and numbness over a part of the tongue and can result in dangerous postoperative aspiration. When necessary, small groups of fibers of the twelfth cranial nerve may be either sectioned or included in a difficult clip placement, which is safer than the aggressive dissection necessary to free them; its use is associated with either no neurological deficit or a trivial one.

Aneurysms of the Vertebral Confluens and Lower Basilar Trunk

Aneurysms of the vertebral confluens and the lower basilar trunk are some of the most difficult aneurysms to treat due to the depth of exposure, the requirement for optimal exposure ventral to the brainstem, and the frequent need for innovative cranial base exposures. As a result, these aneurysms are more commonly treated with endovascular strategies if possible; however, in some circumstances, endovascular strategies are not possible. The vertebral confluens, or the vertebrobasilar junction, is a unique arterial structure where two large vessels join to form a larger artery. This configuration is often very tortuous, involves different calibers and lengths of vertebral arteries, and potentially involves fenestrations of the confluens and lower basilar trunk. As such, these configurations allow complex hemodynamics that predisposes this area to aneurysm development. Aneurysms of the lower basilar trunk are usually associated with the origin of the anterior inferior cerebellar artery (AICA) and the sixth cranial nerve.

The surgical exposure is normally done with the patient in the lateral position. The surgical approach is similar to the far lateral exposure explained previously except the initial dissection is carried out between the fibers of the ninth cranial nerve below and the seventh and eighth cranial nerves above. Exposure of lower basilar trunk usually involves a cranial base approach, either by sectioning the tentorium from a subtemporal approach or by an exposure anterior to or through the sigmoid sinus via a transpetrosal approach.

Conclusion

Intracranial aneurysms continue to provide significant rates of morbidity and mortality despite decades of advanced knowledge, technology, and research. The natural history of unruptured intracranial aneurysms is still controversial, especially with regard to aneurysms smaller than 7 mm. Other morphological factors have been associated with increased rupture risk but no one factor seems able to predict rupture, as would be expected from an entity that likely involves a multifactorial pathogenesis, pathobiology, and pathobehavior. Each individual unruptured aneurysm should be evaluated with all aspects taken into consideration, including lesional characteristics and patient comorbid conditions, as well as patients’ risk aversion and expectations from the management plan.

Contemporary management strategies should involve all aspects of neurovascular care, including neuroendovascular physicians, neurocritical care, and neuroanesthesia. All of these specialties should be synergistic and complementary in their approach with the common goal of managing the obliteration of the aneurysm with minimal risk, both short-term and long-term, to the patient. It is now essential that all centers offering state-of-the-art cerebrovascular medicine have expertise in all specialized aspects of neurovascular care. Without such, we would be doing our patients a disservice.