Operations for Vascular Compressive Syndromes

Introduction

Surgical decompression for arteriovenous compression of the neural elements at the skull base was first described in the early 1900s. After significant refinement of surgical technique over several decades, it has become a popular and durable treatment for pain syndromes such as trigeminal neuralgia (TN), hemifacial spasm (HFS), and glossopharyngeal neuralgia (GN). The general principle underlying these approaches is that vascular compression results in recurrent, intractable pain, and that operative decompression via mobilization of the offending vasculature away from the respective neural element improves symptoms.

At the turn of the twentieth century, Walter Dandy first performed trigeminal nerve sectioning via a retromastoid approach for patients with tic douloureux , now referred to as TN. In 1934, he described his results in 215 patients. This series represented the initial identification of superior cerebellar artery/petrosal vein-related compression of the trigeminal nerve. Due to limitations in surgical technique, the approach did not gain popularity despite some early favorable results. The advent of the operating microscope decades later led to improved operative techniques in multiple domains of skull base surgery. With efforts spearheaded by Peter Janetta in the 1980s, the surgical technique of microvascular decompression was refined and its indications were expanded to compression of the facial and glossopharyngeal nerves.

Vascular compression can occur from either arterial or venous components. The former is more commonly observed. In a series of 55 patients who underwent microvascular decompression (MVD) for TN, 17.5% had primary compression from a venous element. In only 8.3% of patients was venous compression the only etiology, underscoring the predominance of arterial compressive pathology. Although underlying etiologies of vascular compression can be varied, a prevailing pathophysiologic explanation is that long-standing vascular disease including hypertension and arteriosclerosis can result in vascular ectasia. In combination with brain atrophy in the setting of aging, vessels may ultimately be displaced to an abnormal anatomic location. This new, aberrant location may be in close proximity to a cranial nerve: in TN, the trigeminal nerve; in HFS, the facial nerve; and in GN, the glossopharyngeal nerve. Resultant neural compression typically occurs at the nerve root exit/entry zone. Existing at the transition point of central to peripheral myelination patterns, the nerve at its root entry zone is relatively vulnerable due to a lack of epineurium and is protected only be arachnoid matter. ^, Continued pulsatile neural compression leads to stereotyped pain syndromes (as described below) on the basis of nerve irritation, local demyelination, and subsequent electrophysiologic perturbation.

In this chapter, we describe the clinical presentation and management of each of the major vascular compressive syndromes, including TN, hemifacial spasm, and GN. We discuss the pre-, intra-, and postoperative considerations for these patients. We additionally describe our preferred surgical technique.

Vascular Compressive Syndromes

Here, we will describe each of the vascular compressive syndromes, including TN, hemifacial spasm, and GN. Prior to specific discussion, it is important to consider that these syndromes remain clinical diagnoses. Each syndrome has a stereotyped clinical presentation existing within a spectrum of severity. A thorough history including the character and location of pain, frequency of episodes, and triggers is imperative for an accurate diagnosis. Because of the significance of the clinical history, radiographic imaging is not necessary for the clinical diagnosis of vascular compressive syndromes. However, it remains an important part of the workup, as it can demonstrate nonvascular compression (e.g., mass lesion), which can drastically alter an operative plan should a patient be considered for surgery. MRI is the preferred imaging modality. We favor FIESTA (Fast Imaging Employing STeady-state Acquisition) MRI for optimal delineation of cranial nerves within cerebrospinal (CSF) spaces ( Fig. 39.1 ). Other institutions use vascular imaging with 3D reconstructions.