Introduction

Cranial nerve stimulation strategies have been used to treat a variety of diverse conditions that sometimes prove to be unresponsive to conservative medical therapies. These range from depression to seizure to congestive heart failure.^1–3 More specifically, some other indications include atypical facial pain, terminal branch neuralgias, a variety of headache disorders (i.e., cluster, migraine, trigeminal autonomic cephalalgias, cervicogenic headache, hemicrania continua, trigeminal neuralgia), depression, and postherpetic neuralgia.^1,4–24 Stimulation technology has also been used in a case series to treat central hypoventilation syndrome by stimulation of the phrenic nerve.

This chapter focuses on complications reported during peripheral (distal) stimulation of cranial nerves, namely the terminal branches of the trigeminal nerve, the trigeminocervical complex, and the vagus nerve. Although epidural trigeminocervical complex stimulation has been reported to treat trigeminal neuralgia,²⁵ the reader is directed to Chapter 1 for discussion of complications of epidural spinal cord stimulation (SCS).

Experience with cranial nerve stimulation, compared to SCS or deep brain stimulation, is in its infancy, as suggested by the paucity of literature. Stimulation of the trigeminocervical complex via the occipital nerve, on the other hand, is well described. As one can expect, correlates can be made to patient selection for peripheral cranial nerve stimulation and SCS. The procedure is contraindicated in patients with local infection near the injection site, coagulopathy, allergy to injectate or components of the device, comorbidities or conditions that prevent fluoroscopic needle guidance, or an inability to provide consent. Furthermore, future requirement for magnetic resonance imaging should be elicited.

Although a review of the American Society of Regional Anesthesia’s 2010 guidelines for neuraxial interventions may not directly be applicable to peripheral branch of cranial nerve stimulation interventions, concurrent use of anticoagulants before surgery may increase the bleeding risk. Therefore it is advised that readers familiarize themselves with these guidelines, as well as the guideline statements of perioperative use of anticoagulant therapy.²⁶

Patient selection guides treatment success. Psychometric testing for neuromodulation candidacy deserves special mention. It is well established that concurrent psychiatric illness reduces interventional treatment success rates²⁷ and that approximately 20% to 45% of pain patients have accompanying psychopathology.²⁸ Therefore it is essential that appropriate measures be taken to diagnose, treat, or exclude unsuitable candidates. Instruments described to aid in identifying the presence of clinically significant psychopathology include the Symptom Checklist 90 (SCL-90-R) and the Minnesota Multiphasic Personality Inventory (MMPI-2). Poor treatment outcome was identified in patients with presurgical somatization, depression, anxiety, and poor coping.²⁹

Of paramount significance, and similar to SCS, the current constraints and limitations of the current neuromodulatory technology requires vigilance and as a consequence of changes in impedance and battery life, either reprogramming or surgical revision. Simply stated, these devices require long-term management because these are lifelong therapies.

Furthermore, appropriate training within Accreditation Council for Graduate Medical Education (ACGME) accredited programs and mentorship is essential to ensure treatment success and limit iatrogenic morbidity; inadequately trained providers attempting to use these therapies will not only potentially harm their patients but will also broadly limit access to these therapies by undermining patient outcomes.

Background

Trigeminal stimulation techniques have been described both centrally and peripherally; however, more reliable stimulation has been achieved in the latter.⁴ Furthermore, because overall complications of central trigeminal gasserian stimulation have been reported to be near 30% to 40%^30–32 and with reduced complications with peripheral branch stimulation, enthusiasm for central stimulation has dwindled. The trigeminal nuclear systems are bilateral structures that span from the midbrain to the medulla. The caudal-most portion, the trigeminal nucleus caudalis, may extend down as far as the second or third cervical level, which has both anatomic and clinical implications. Goadsby³³ demonstrated the presence of convergence between the cervical and trigeminal system, forming a trigeminocervical complex. This was characterized by Anthony³⁴ and helped form the basis for greater occipital nerve stimulation for treatment of headache (Fig. 3-1). Traditionally, stimulation was achieved by using either implanted cylindrical or paddle leads. There are some reports of using a small implantable device without the traditional implantable pulse generator (IPG) placement¹⁰ along with transcutaneous electrical nerve stimulation unit applications.¹¹

Fig. 3-1 Illustration of the trigeminocervical complex (A) and stimulator placement (B to D) using midline and retromastoid approaches. SCM, sternocleidomastoid muscle.

(Part A modified from Anthony M: Headache and the greater occipital nerve, Clin Neurol Neurosurg 94(4):297-301, 1992; part B modified from Kapural L, Mekhail N, Hayek SM, et al: Occipital nerve electrical stimulation via the midline approach and subcutaneous surgical leads for treatment of severe occipital neuralgia: a pilot study, Anesth Analg 10:171-174, table, 2005; part C modified from Oh MY, Ortega J, Bellotte JB, et al: Peripheral nerve stimulation for the treatment of occipital neuralgia and transformed migraine using a C1-2-3 subcutaneous paddle style electrode: a technical report, Neuromodulation 7:103-112, 2004; part D modified from Trentman TL, Zimmerman RS: Occipital nerve stimulation: technical and surgical aspects of implantation, Headache Currents 48(2)319-327, 2008.)

Peripherally, the trigeminal nerve terminates as the supraorbital and supratrochlear nerve from V1, the infraorbital nerve from V2, and the mental nerve from V3. These sites lend themselves to subcutaneous neurostimulatory targets (Fig. 3-2).^{4,6,12,17,18,24,35,36}

Fig. 3-2 A, Terminal branches of the trigeminal nerve.

(From Brown DL: Atlas of regional anesthesia, ed 3, Philadelphia, WB Saunders, 2006.)

B, Stimulator lead placement.

(Modified from Slavin KV, Wess C: Trigeminal branch stimulation for intractable neuropathic pain: technical note, Neuromodulation 8(1):7-13, 2005.)

Vagal nerve stimulation (VNS) has been approved for drug-refractory epilepsy and is a viable option for those who decline surgery or nonsurgical candidates. Its safety and efficacy have been well established.³⁷ Furthermore, it has been used in the treatment of people with treatment-resistant depression. Commonly, the left vagus nerve is stimulated, not with the commonly used spinal cord stimulator but via a NeuroCybernetic Prosthesis.³⁸ The exact mechanism of action is unknown, although it is postulated to involve vagal sensory afferents. Whereas high-frequency stimulation causes electroencephalographic desynchronization, low-frequency stimulation causes synchronization.³⁹ Typically, the VNS is positioned on the left side because right-sided stimulation causes more cardiac slowing as a consequence of sinoatrial (SA) node stimulation.⁴⁰ Although this is not commonly used to treat pain, the scope is broadening.^35,41,42 Therefore, VNS is discussed here briefly for completeness.

Although there is commonality with these approaches to cranial nerve stimulation, their indications, operative considerations, and surgical approaches are divergent. Therefore occipital nerve stimulation, peripheral trigeminal nerve stimulation, and VNS are considered here separately and sequentially.