OA-PICA Bypass

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9 OA-PICA Bypass

Introduction

Yasargil et al.1 demonstrated the feasibility of EC-IC bypass surgery in 1967 after performing the first successful superficial temporal artery to middle cerebral artery anastomosis. Ausman and colleagues2 applied these techniques for vertebral artery (VA) occlusive disease and reported the first intracranial posterior circulation revascularization procedure in 1976 after performing an occipital artery (OA) to posterior inferior cerebellar artery (PICA) anastomosis. Posterior circulation bypass surgery has since been used to treat vertebrobasilar insufficiency, skull base tumors involving the VA and its branches, and complex or giant posterior circulation aneurysms. Current advances in endovascular techniques and the availability of intracranial stents have largely limited the need for posterior circulation bypass surgery for vertebrobasilar insufficiency. Occipital artery–PICA bypass surgery, however, remains a valuable tool in the management of fusiform aneurysms of the VA encompassing the PICA origin as well as giant and complex VA/PICA and PICA aneurysms that cannot be reconstructed with surgical clipping or endovascular coiling and require parent artery occlusion or trapping. In the context of VB insufficiency, the bypass may still have a role in the rare settings of poor endovascular access due to tortuosity or occlusion. This chapter reviews the relevant anatomy, surgical technique, perioperative care, and complications associated with OA-PICA revascularization.

Anatomy

Occipital Artery

The OA is an ideal choice for PICA revascularization as it can be encountered during the suboccipital approach and closely approximates the size of the PICA. The course of the OA can be divided into three segments.3

The first segment, also known as the digastric segment, extends from the origin of the OA from the external carotid artery to the point of emergence from the occipital groove of the mastoid process. The OA originates from the posterior or lateral wall of the external carotid artery at the level of the angle of the mandible. The artery ascends medial to the external carotid artery and lateral to the internal jugular vein to a point posterior and medial to the styloid process. The OA then courses posteriorly and laterally superficial to the rectus capitus lateralis muscle first and then superior oblique muscle.4 The artery is covered by the posterior belly of the digastric muscle laterally, hence known as the digastric segment. The artery then runs in the occipital groove or occasionally a true bony canal3 medial to the mastoid notch, in which the posterior belly of the digastric muscle arises.4

The second segment, also known as the suboccipital or horizontal segment, extends from the emergence of the OA from the occipital groove of the mastoid process to the superior nuchal line. The OA exits the occipital groove between the superior oblique muscle and posterior belly of the digastric and is covered by the splenium capitis and sternocleidomastoid. The artery courses medially in a horizontal plane either superficial or deep to the longissimus capitus muscle, depending on whether the occipital groove is absent or present. The OA then continues superficial to the semispinalis capitis muscle just below the superior nuchal line in the upper part of the posterior triangle. The artery then changes course and runs vertically upward, piercing the fascia connecting the cranial attachment of the trapezius and sternocleidomastoid muscles to the superior nuchal line.5 The suboccipital segment gives rise to ascending and descending muscular branches as well as transosseous branches to the dura of the posterior fossa. The diameter of the suboccipital segment ranges from 1.6 to 2.2 mm (mean 1.9 mm) and the length ranges from 75 to 85 mm (range 79.3 mm).6

The third segment, also known as the occipital or subgaleal segment, begins at the superior nuchal line after the OA pierces the fascial attachment of the trapezius and sternocleidomastoid muscles. In a cadaveric study, the OA was found to cross the superior nuchal line approximately 35 mm (±0.5 mm) lateral to the inion.3 The artery continues underneath the galea and above the occipitalis muscle before dividing into its terminal branches. The diameter of the OA at the superior nuchal line is approximately 1.4 mm (±0.3 mm).3

PICA Artery

Segments of the PICA

It is very convenient and appropriate to subscribe to the concept advanced by Lister et al.,7 that the PICA can be divided into five segments based on its relationship to the medulla and the cerebellum: anterior medullary, lateral medullary, tonsillomedullary, telovelotonsillar, and cortical.

The anterior medullary segment begins at the origin of the PICA from the VA anterior to the medulla oblongata. Congenital anomalies of the PICA include double origin, fenestration, or duplicated PICAs, a common anterior inferior cerebellar artery (AICA)–PICA configuration, a VA termination at the PICA, extradural origins at C1 and C2 levels (5% to 20%), origins at the hypoglossal, proatlantal, or posterior meningeal arteries, and at all points along the intradural VA.815 From its origin, the artery runs posteriorly around the medulla past the exit of the hypoglossal nerve rootlets from the anterior border of the inferior olivary complex to the boundary between the anterior and lateral surfaces of the medulla, which is marked by a rostrocaudal line through the most prominent part of the inferior olive. The lateral medullary segment begins at the point where the PICA passes the most prominent part of the inferior olive and extends posteriorly around the lateral aspect of the medulla to the origin of the glossopharyngeal, vagus, and accessory rootlets from the posterior border of the inferior olivary complex. The PICA continues medially as the tonsillomedullary segment between the lower half of the cerebellar tonsil and the posterior aspect of the medulla oblongata. The artery makes a caudally convex curve as it passes around the lower pole of the cerebellar tonsil known as the caudal or infratonsillar loop. The caudal loop is frequently used as a recipient during OA-PICA bypasses and its diameter ranges from 0.9 to 1.4 mm (mean 1.2 mm).6 After forming the caudal loop, the PICA ascends to the midlevel of the medial surface of the tonsil where it becomes the telovelotonsillar segment. The artery continues along the medial surface of the tonsil toward the roof of the fourth ventricle. The PICA then forms a rostrally convex curve referred to as the cranial or supratonsillar loop. This loop consists of proximal ascending and distal descending limbs and an apex that lies caudal to the fastigium at the center of the inferior medullary velum. The ascending limb runs posterior to the tela choroidea and inferior medullary velum toward the fastigium of the fourth ventricle. The descending limb runs posteriorly in the fissure between the vermis medially and the superomedial surface of the tonsil and cerebellar hemisphere laterally. The PICA emerges from the fissure and continues as the cortical segment. The artery divides into a smaller medial and a larger lateral trunk and subsequently gives rise to hemispheric, vermian, and tonsillar branches.

Branches of the PICA

The PICA gives rise to three types of branches:7

Preoperative evaluation

Preoperative evaluation includes standard preoperative labs, an electrocardiogram, a chest radiograph, and assessment of the patient’s general health. In contrast to dissection of the superficial temporal artery, harvesting the OA requires considerable muscle dissection and may lead to postoperative hematomas particularly if patients are on aspirin. We therefore do not give patients aspirin preoperatively and prefer to stop aspirin 1 week prior to surgery in patients on aspirin therapy for vertebrobasilar insufficiency.

Digital subtraction cerebral angiography with three-dimensional reconstruction as well as selective external carotid artery injections is essential. Aneurysm size, morphology, dome-to-neck ratio, and relation to the surrounding arteries are evaluated. The caliber and course of the OA as well as the caliber and configuration of the PICA vessel and its tributaries should be carefully studied. The course, position, and proximity of the tonsillomedullary segments of both PICAs need assessment, in order to have a side-to-side PICA-PICA bypass as an alternate plan. In cases of vertebrobasilar insufficiency, the caliber of both VAs and the presence and caliber of the posterior communicating arteries must be evaluated and if necessary an Alcock’s test should be performed (carotid compression during vertebral artery injection).

Physiological imaging modalities such as positron emission tomography, xenon computed tomography, single-photon emission computed tomography, computed tomography perfusion, and magnetic resonance perfusion commonly used to detect hemodynamic compromise in anterior circulation occlusive disease are less effective in assessing the posterior circulation as a result of their limited regional resolution.16 Furthermore, the validity of these imaging modalities in detecting posterior circulation hypoperfusion remains uncertain. Phase-contrast quantitative magnetic resonance angiography (QMRA) has become available in recent years and is capable of directly measuring volumetric blood flow (milliliters per minute) through the major vessels of the posterior (as well as anterior) circulation. The technique is now implemented and enhanced in commercially available software called the NOVA (Noninvasive Optimal Vessel Analysis) system (VasSol, Inc., Chicago, IL). Table 9–1 shows the mean blood flow values and ranges for posterior circulation vessels in 50 healthy patients.17 In a retrospective study of 47 patients with symptomatic vertebrobasilar disease, patients with >20% reduction of blood flow in the basilar artery (<120 cc/min) and PCAs (<40 cc/min) had a higher risk of stroke as compared to patients with preserved blood flow.17 The VERiTAS (Vertebrobasilar Flow Evaluation and Risk of Transient Ischemic Attack and Stroke) is an ongoing prospective multicenter observational study funded by the National Institutes of Health and aimed at determining the utility of QMRA in assessing patients with symptomatic vertebrobasilar occlusive disease of ≥50%. If predictive, QMRA evaluation could help identify high-risk patients who would benefit most from either surgical revascularization or endovascular angioplasty and stenting.

Table 9–1 The Mean Value and Ranges of Blood Flow for Posterior Circulation Vessels in 50 Healthy Volunteers.

Vessel Mean Flow (cc/min) Range* (cc/min)
BA 190 150–230
LPCA 72 50–94
RPCA 68 50–86
LVA 126 94–158
RVA 110 81–139

BA, indicates basilar artery; PCA, posterior cerebral artery; VA, vertebral artery; L, left; R, right.

* Mean ± standard deviation.

Surgical indications

Indications for cerebral revascularization procedures can be divided into flow augmentation and flow replacement.

Anesthetic technique and neuroprotection

The surgery is performed under general anesthesia. Hypotension must be avoided during the initial part of the procedure particularly in patients with marginal cerebral perfusion. Hyperventilation and alpha-adrenergic agents are not recommended because of their vasoconstrictive effects. We routinely use modest hypothermia (33°C) throughout the procedure as well as induced blood pressure elevation to 20% to 30% of baseline during the period of temporary PICA cross-clamping to augment collateral flow. Electrophysiologic monitoring using somatosensory and motor-evoked potentials and brainstem auditory-evoked potentials allows early detection of ischemia or excessive retraction and manipulation. Barbiturates have been used during bypass surgery to increase tolerance to cerebral hypoperfusion. The mechanisms of barbiturate neuroprotection are multifactorial and incompletely understood. It is believed that a reversible, dose-dependent depression of cerebral blood flow occurs, with subsequent reduction in cerebral metabolic rate and intracranial pressure.1821 Furthermore, vasoconstriction in normal areas of the brain may result in an inverse steal phenomenon with redistribution of cerebral blood flow to ischemic tissue.22 At a cellular level, barbiturates have been demonstrated to reduce ischemia-induced glutamate release,23 enhance GABA-ergic transmission,24,25 and reduce ischemia-induced intracellular calcium through inhibition of both voltage-gated calcium channels and NMDA receptors.26

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