Percutaneous Stereotactic Rhizotomy in the Treatment of Intractable Facial Pain

Step 1: Cannulation of the Foramen Ovale

One hour before the procedure, 0.4 mg of atropine is administered intramuscularly to reduce oral secretions and prevent bradycardia. The patient is positioned supine on the fluoroscopic table with the head neutral. Next, Hartel’s three anatomic landmarks are plotted on the face: a point beneath the medial aspect of the pupil, a point 3 cm anterior to the external auditory meatus, and a point 2.5 cm lateral to the oral commissure ( Fig. 115.1A and B ). The first two points provide the rostral/caudal and medial/lateral trajectories for the penetration of the foramen ovale, and the third point is where the needle penetrates the skin of the jaw. The affected cheek is prepared with Betadine (Purdue-Frederick, Norwalk, CT). A 21-gauge spinal needle placed in the deltoid subcutaneous tissue acts as a reference and grounding electrode, or alternatively, a Bovie pad can be used.

Before cannulation of the foramen, understanding the skull base anatomy and its anatomic variants is essential ( Fig. 115.2 ). Aberrant placement of the cannula can result in unintended neurovascular injuries. Use of lateral fluoroscopic imaging will aid in avoiding the following: cannulation of the inferior orbital fissure (IOF) anterosuperiorly or the jugular foramen posteroinferiorly, or intracranial placement of the cannula through aberrant foramina (e.g., foramen of Vesalius, which lies anteromedial to the foramen ovale, or innominate canal of Arnold, which lies posterior to the foramen ovale). Pulsatile blood flow through the cannula indicates penetration of the internal carotid artery (ICA). Puncture of the ICA can occur in three locations: at the proximal C2 segment at the carotid canal, the C3 segment with the electrode passing through the cartilage of the foramen lacerum, and the cavernous (C4) segment ( Fig. 115.3 ). This third type of penetration, described by Rish, occurs when an anteromedial electrode passing through the foramen ovale penetrates the C4 segment of the ICA; ischemic complications, such as hemiparesis, and carotid-cavernous fistula, have resulted from puncture of the ICA. If ICA injury occurs, the cannula is withdrawn promptly, manual pressure is applied over the posterior pharyngeal space, the procedure is discontinued, and the patient is allowed 24 to 48 hours to convalesce. Generally, arterial punctures are minimized by refraining from broad angular readjustments of the electrode and diligent attempts to avoid trajectories that are either posterolateral or posteromedial to the foramen of ovale; such trajectories jeopardize the carotid canal and foramen lacerum, respectively.

The primary goal of the cannulation step is penetration of the medial portion of the foramen ovale and placement of the electrode tip in the retrogasserian rootlets ( Fig. 115.4 ). Using Härtel’s landmarks, we advocate either the direct penetration technique or the sequential palpation in which the surgeon sequentially walks the cannula down the smooth surface of the infratemporal fossa toward the superior-medial aspect of the foramen ( Fig. 115.5 ). If the cannula enters the posterolateral aspect of the foramen, it may elude the trigeminal cistern and not contact the trigeminal ganglion within its dural investment. As the electrode is advanced, it may not reach the maxillary or ophthalmic divisions of the rootlet.

To begin, a 9-mm airway turned sideways or a bite block is inserted into the patient’s mouth between the molars on the opposite side to prevent the patient from involuntarily biting the surgeon’s finger. The patient is anesthetized with a rapid intravenous injection of 30 to 50 mg of methohexital (Brevital) followed by a 10-mL saline flush. Once the patient is fully asleep, the surgeon inserts the index finger of gloved hand inside the patient’s mouth, sliding along the inferior and medial wall of the lateral pterygoid to a point where it hooks around the lateral pterygoid, to guide the cannula toward the foramen ovale. A standard 100-mm, 20-gauge cannula, with its stylet in place, is inserted into the cheek 2.5 cm lateral to the oral commissure. The cannula is aimed toward the intersection of an axial plane, passing 3 cm anterior to the external auditory meatus, and a sagittal plane, passing through the medial aspect of the pupil. Although placement is by free-hand manipulation, fluoroscopic visualization is important to assist localization. Use of the image intensifier in the lateral plane effectively localizes the needle.

Entrance of the cannula into the foramen ovale is signaled by a wince and a brief contraction of the masseter muscle, indicating contact with the mandibular sensory and motor fibers. Before the cannula is advanced any further, a lateral fluoroscopic image is obtained to confirm proper placement in the foramen ovale ( Fig. 115.6 ). Fluoroscopy allows targeting a point along the lateral projection of the clivus, which is 5 to 10 mm below the floor of the sella. If difficulty penetrating the foramen ovale ensues, one should pause and return to a fundamental principle—namely, the safest approach to the foramen ovale is a trajectory that begins anteromedially to the foramen. In this manner, the surgeon can sequentially palpate, using the cannula along the smooth surface of the infratemporal fossa, and enter the superior medial aspect of the foramen. Use of this technique ensures a cannula trajectory in which the electrode will enter the trigeminal cistern at an angle and then sequentially contact each of the three divisions of the trigeminal root. Furthermore, targeting the anteromedial portion of the foramen ovale reduces the risks associated with probing alternative portions of the skull base, lowers the incidence of hematoma due to venous or arterial hemorrhage, and increases the probability of entering the trigeminal cistern.

Proper positioning of the cannula within the trigeminal cistern allows free flow of cerebrospinal fluid (CSF) through it in most patients, except for the few who have undergone previous surgical procedures or chemical injection. However, egress of CSF does not ensure that the cannula lies in the proper position (retrogasserian). CSF can also be obtained either from the infratemporal subarachnoid space if the needle is too deep or from the region distal to the gasserian ganglion if the dural subarachnoid sleeve extends beyond the rootlets. Fluoroscopy must ascertain that the trajectory does not either project anterior to the sella where the cannula may penetrate the IOF or lie too low on the clivus (more than 15 mm) where entry into the jugular foramen may occur.

If satisfied with the position of the cannula and the flow of CSF, a small clamp at skin level holds the cannula in place to prevent its further advancement into the trigeminal ganglion. The surgeon removes the bite block and introduces the electrode into the cannula. The cable, which connects the electrode to the stimulator, should be connected to the electrode before its insertion. If connected after it is in the cannula, the electrode can vibrate within the trigeminal nerve root and elicit a trigeminal attack.

Step 2: Stimulation of the Trigeminal Nerve

Subtle adjustments in the position of the electrode tip facilitate precise stimulation of the division of the trigeminal root. When making an adjustment or generating stimuli, the surgeon has two important objectives. First, precisely reproduce the pattern of the patient’s trigeminal pain. An appropriate stimulus that effectively replicates the pain will lessen the likelihood of lesions in adjacent divisions. Precise stimulation is principally related to electrode tip placement (as described below). Second, identify the intensity threshold used to reproduce the patient’s typical pain, so that the neurosurgeon can judge the duration and temperature needed to generate an effective partial sensory lesion as described later.

Targeted stimulation begins by manipulating the electrode’s tip in two dimensions as viewed on lateral fluoroscopy: the relationship of the electrode tip to the profile of the clivus and the curvature of the electrode’s tip. When the tip rests at the clival level, a stimulating pulse typically elicits paresthesias in the maxillary division rootlets. Advancement beyond the clival profile moves the electrode into the territory of the ophthalmic division rootlets, while withdrawal of the needle from the level of the clivus targets the mandibular division rootlets ( Fig. 115.7A ). The electrode’s tip should not be advanced more than 10 mm deep to the profile of the clivus because the tip can contact the trochlear or abducens nerve in this region. Sometimes the needle must be redirected more anteromedially to bring the tip closer to the posterior clinoid process for closer contact with the ophthalmic division. If the globe moves during stimulation, the cannula is too near the cranial nerves (CNs) in the cavernous sinus or perhaps near the brain stem. Stimulus-evoked facial contractions indicate that the electrode is either too deep, inclined too low on the clivus, or the stimulation level is too high. A lesion should not be made if there is any indication of motor nerve III, IV, VI, or VII stimulation or arterial bleeding.

After this initial placement and understanding of clival relationships, the axial rotation of the curved electrode permits a secondary form of targeting. Precise anatomic localization within the sensory root is aided by this maneuverability. The curved electrode tip is a coil spring that carries a thermocouple, stimulator, and lesion-generating probe. When the electrode is fully inserted into the cannula, the curved tip extends 5 mm beyond the end of the cannula and projects 3 mm perpendicular to the long axis of the electrode. Insulation of the cannula with polytetrafluoroethylene allows only the extruded portion of the electrode (0 to 5 mm) to be conductive. Rotation of the electrode can occur through a 360-degree axis for stimulation and lesion production ( Fig. 115.7A ). However, final placement of the electrode’s tip is determined by the patient’s response to electrical stimulation. In the sagittal plane, which can be viewed on lateral fluoroscopy, a tip projecting cephalad or medial provides better access to the fibers of the ophthalmic division, whereas the caudal or lateral projection should enable contact with the mandibular fibers. Additionally, if the electrode contacts the motor root and elicits stimulation of the masseter or pterygoid muscles, the electrode can be rotated laterally to reduce the incidence of a lesion that may result in a trigeminal motor paresis.

Because feedback is important at this point, the patient is awakened to begin stimulation of the trigeminal nerve. Stimulation settings begin at 0 volts (V) with 50 pulses/s for 1-ms duration (Cosman Radiofrequency Generator); however, settings can vary based on the stimulator. Voltage is gradually increased until the patient experiences paresthesias in the same general pattern as the trigeminal neuralgia. Typically 0.1 to 0.4 V are required to reproduce the pain pattern in most patients. Stimulation at higher voltage (0.5 to 1.0 V) may be needed in patients who have had previous intracranial rhizotomy or repeated alcohol injections. If 1.0 V is reached without eliciting the typical pain pattern, stimulation is discontinued and the cannula repositioned. For this portion of the procedure, cooperation is important so the patient must be calm and not in pain. If a patient becomes very emotional or cannot comply, observation of the response to stimulation is sufficient.

Alternatively, stimulation can be achieved with mild heat (<50°C). The evoked response not only localizes but reliably indicates the probe temperature required for lesion production. Consequently, the threshold current responsible for eliciting pain can be translated into a temperature and duration for the initial lesion, thus meeting our second objective. Our paradigm to convert a stimulus threshold voltage into a temperature and duration for an initial lesion is found in Table 115.1 .

Step 3: Lesion Production

Studies have shown a direct correlation between the extent of facial sensory deficit and the duration of trigeminal pain relief with percutaneous stereotactic radiofrequency rhizotomy. However, large sensory deficit also leads to a higher incidence of complaints (e.g., problems eating) and dysesthesia ( Table 115.2 ). Generation of a lesion with mild to moderate hypalgesia in the primarily affected division(s) provides sufficient longevity yet limits the morbidity associated with more dense lesions. For a patient who has not had a previous procedure, we recommend producing a mild hypalgesic lesion (<50% loss of pain perception with preservation of touch perception) in the involved trigeminal division. For a patient with pain recurrence after previous procedures have failed, we recommend producing a major or dense hypalgesic lesion (>75% loss of pain perception with preservation of touch perception) in the involved trigeminal division. The ease of performing the procedure allows for additional treatments in patients with recurrent pain.

With the information gained during stimulation, additional intravenous anesthetic is administered and a preliminary lesion is produced. Reproducible lesions are 5 × 5 × 4 mm, are eccentric, and orient toward the curve of the electrode. The electrode tip measures 0.5 mm in diameter. A thermocouple sensor located at this tip provides calibration accuracy of ±2°C over a range of 30°C to 100°C. During lesion production, pinprick sensory testing should be continuous to determine when a deficit begins to develop. A facial flush (secondary to antidromic release of vasodilatory neuropeptides, such as substance P and calcitonin gene-related peptide), may be seen and is localized to the division of the trigeminal nerve undergoing thermal lesioning.

After the initial lesion, when the patient is fully awake, sensory testing of the face is conducted to assess numbness. Testing follows a standard regimen that includes verbal feedback from the patient and observation by the surgeon. Gross pinprick sensation is tested in all three divisions on both sides of the face by marching a pin toward and then across midline. If any difference is noted between left and right sides, the patient uses a 10-point scale to rate the extent of numbness on each side. We then test for analgesia by comparing pinprick to light touch. Because of overlap among the sensory distributions of the trigeminal nerve, a keen knowledge of the autonomous areas of sensory innervation is fundamental for proper sensory assessment ( Fig. 115.7B ).

Lesion production is repeated until the desired effect is achieved. After creation of an initial lesion using our paradigm, subsequent lesions of 60- to 90-second duration are made by increasing the temperature 5°C with each sequential lesion. When moderate hypalgesia is approached, great care is exercised to avoid overshooting the desired result, which includes preservation of light sensory touch. Production of additional lesions can often be made without the use of additional anesthetic agent and should be done with constant sensory testing for fine control of the degree of sensory denervation. This tactic is particularly valuable when it is imperative to avoid analgesia and to preserve CN sensitivity (as for a V1 lesion).

After achieving the desired sensory loss, the patient is observed for an additional 15 minutes. If the examination indicates a stable level of hypalgesia, the distribution and degree of sensory deficit in addition to the function of the masseter, pterygoid, facial, and ocular muscles is recorded. The patient is returned to a regular room and is observed for at least 2 hours. During this period, the patient and family are informed of the requisite eye care, chewing exercises, and the consequences of facial hypalgesia. Tapering of anticonvulsant medications begins upon discharge and is completed by 1 to 2 weeks after surgery.