Reason Of Pain In Lower Anterior Teeth And Lip After Rftc And Mental Block

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Blockade of the SPG is used in the treatment of many painful medical syndromes involving the face and head. Sluder was the first to describe in the literature a unilateral facial pain at the root of the nose, which sometimes spread retro-orbitally toward the zygoma and extended back to the mastoid and occiput.13 The pain was commonly associated with parasympathetic features such as lacrimation and rhinorrhea, with or without mucosal congestion.13 Sluder called this pain syndrome sphenopalatine neuralgia. He believed the the cause of this pain was the spread of infection from the paranasal sinuses, which caused irritation of the SPG. This was initially accepted as a possible causal mechanism but was questioned when other syndromes, such as low back pain, sciatica, and dysmenorrhea, were attributed to irritation of the SPG. In the early 1940s, Eagle13 sought to revive interest in sphenopalatine neuralgia when he presented his thesis to the American Laryngological, Rhinological, and Otological Society. He agreed with Sluder on the existence of sphenopalatine neuralgia but disagreed with him on the etiology of the disorders Eagle believed that intranasal deformities such as deviated septum, septal spurs or ledges, and prominent turbinates were responsible for irritation of the ganglion, which caused pain. Others have believed that a reflex vasomotor change or possibly a vasomotor syndrome might be responsible for causing the pain.3 Regardless of the proposed causes, sphenopalatine neuralgia is an indication for SPGB.

Trigeminal neuralgia is a second indication for SPGB. Ruskin, in 1925, disagreed with Sluder on the indication for SPGB and instead proposed the involvement of the SPG in the pathogenesis of trigeminal neuralgia.151 As discussed in the anatomy section of the chapter, the SPG is directly connected to the maxillary branch of the trigeminal nerve via the pterygopalatine nerves. Ruskin believed that blockade of the SPG would in turn relieve the symptoms associated with trigeminal neuralgia via a retrograde effect. There are few case reports in current literature that support this theory.16

Although new medications for the treatment of migraine and cluster headache are introduced yearly, there are small subsets of patients who fail to respond to oral and parenteral dosing and are forced to seek alternative methods for pain control. Blockade of the SPG has been used in such cases with varying success.13 m 13

Another indication for SPGB is atypical facial pain. The pain is usually unilateral and described as constant, aching, burning and not confined to the distribution of a cranial nerve.113 The entire face, scalp, and neck may be involved. The pain may have a sympathetic component, which makes SPGB ideal, because the postganglionic sympathetic nerves pass through the ganglion.

Other reported uses of SPGB include back pain, sciatica, angina, arthritis, herpes zoster ophthalmicus, and pain from cancer of the tongue and the floor of the mouth.113 113 113 These are not "true" indications for SPGB but instead reveal the resourcefulness of this block for cases in which conventional therapies are ineffective.

Anatomy and Physiology

The sphenopalatine ganglion is the largest group of neurons outside of the cranial cavity. It lies in the pterygopalatine fossa, which is approximately 1 cm wide and 2 cm high and resembles a "vase" when seen on a lateral fluoroscopic view. The pterygopalatine fossa is bordered anteriorly by the posterior wall of the maxillary sinus, posteriorly by the medial plate of the pterygoid process, medially by the perpendicular plate of the palatine bone, superiorly by the sphenoid sinus. Laterally, it communicates with the infratemporal fossa.112 The foramen rotundum, through which the maxillary branch of the trigeminal nerve passes, is located on the superolateral aspect of the pterygopalatine fossa, whereas the opening to the pterygoid canal, which houses the vidian nerve, is located on the inferomedial portion of the fossa. The ganglion within the fossa is located posterior to the middle turbinate of the nose and lies a few millimeters deep to the lateral nasal mucosa. Also contained within the fossa are the maxillary artery and its multiple branches. The maxillary branch of the trigeminal nerve exits the cranial vault through the foramen rotundum and is located cephalad and slightly lateral to the pterygopalatine fossa.

The sphenopalatine ganglion is a complex neural center with multiple connections. It is "suspended" from the maxillary branch of the trigeminal nerve at the pterygopalatine fossa via the pterygopalatine nerves and lies medial to the maxillary branch when viewed in the sagittal plane ( Fig. 40-1 ). Posteriorly, it is connected to the vidian nerve, also known as the nerve of the pterygoid canal, which is formed by the greater petrosal and deep petrosal nerves. The ganglion itself has efferent branches and forms the superoposterior lateral nasal and pharyngeal nerves. Caudally, the ganglion is in direct connection with the greater and lesser palatine nerves.

As the second largest neural center in the head, the ganglion has sensory, motor, and autonomic components.1151 The sensory fibers arise from the maxillary nerve, pass through the SPG, and are distributed to the nasal membranes, the soft palate, and some parts of the pharynx.12 A few motor nerves are also believed to be carried with the sensory trunks. The autonomic

Pterygopalatine Region

Figure 40-1 Lateral radiographic view of the region surrounding the pterygopalatine fossa. a, pterygopalatine fossa; b, sella turcica; c, maxillary sinus; d, mandible; e, maxilla; and f, zygoma.

innervation is more complex. The sympathetic component begins with preganglionic sympathetic fibers originating in the intermediolateral gray columns of the upper thoracic spinal cord, forming the white rami communicantes, coursing through the sympathetic chain, and ending in the superior cervical sympathetic ganglion. Here, the preganglionic fibers synapse with the postganglionic fibers. The postganglionic fibers then join the carotid nerves before branching off and traveling through the deep petrosal and vidian nerves. The postganglionic sympathetic nerves continue their path through the sphenopalatine ganglion on their way to the lacrimal gland and the nasal and palatine mucosa. The parasympathetic component has its preganglionic origin in the superior salivatory nucleus and then travels through a portion of the facial nerve (VII) before forming the greater petrosal nerve. The greater petrosal nerve in turn joins the deep petrosal nerve to form the vidian nerve, which ends in the sphenopalatine ganglion. Within the ganglion, the preganglionic fibers synapse with their postganglionic cells and continue on to the nasal mucosa, and one branch travels with the maxillary nerve to the lacrimal gland.

Pathophysiology

The role of the sphenopalatine ganglion in the pathogenesis of pain still remains controversial. Sluder2 believed that paranasal sinus infections caused irritation of the ganglion with resulting pain, whereas Eagle13 thought that nasal deformities were responsible for the irritation of the ganglion, which, in turn, caused pain. Ruskin13 advocated the involvement of the SPG in the pathogenesis of trigeminal neuralgia; the exact etiology of this disorder also remains to be defined. Another hypothesis is that a dysequilibrium between the sympathetic and parasympathetic tone within the ganglion result causes the release of substance P or a blockade of local enkephalins.113 Still another hypothesis revolves around the belief that focal demyelination within the ganglion produces abnormal impulses in the afferent nociceptive C fibers which lead to pain.™ Friedman3 suggested that local dilatation of the internal maxillary artery is the source of irritation of the SPG. A general consensus regarding the role and pathogenesis of the SPG remains elusive.

Methods of Blockade

The SPG can be blocked by several techniques. The drugs frequently used are local anesthetics (4% cocaine, 2% to 4% lidocaine, or 0.5% bupivacaine/ropivacaine/levobupivacaine), depot steroids (methylprednisolone or triamcinolone diacetate), with or without 6% phenol. To prolong the blockade, radiofrequency thermocoagulation (RFTC) can be employed, and more recently at our institution, electromagnetic field (EMF) pulsed radiofrequency lesioning has been used. The current hypothesis regarding the mechanism of action of EMF is that the membrane of nerves has a capacitor function and that EMF creates a high electric field, which punches holes in the capacitor and thus blocks transmission of stimuli through A delta and nociceptive C-fibers.113 Informed consent must be obtained and complications must be explained before the block. Patients taking oral anticoagulants should stop these several days before the procedure as long as it is not detrimental to their health. Bleeding parameters should be obtained to confirm normal values.

Techniques of Blockade

TECHNIQUE ONE: INTRANASAL TOPICAL APPLICATION OF LOCAL ANESTHETIC ( Fig. 40-2 )

The intranasal topical application of local anesthetic is relatively easy to perform and can be taught to the patient if effective. A 3.5-inch cotton tip applicator is dipped in the anesthetic solution (cocaine or lidocaine).113 113 The applicator is inserted through the ipsilateral nare on the affected side while a parallel line is maintained with the zygomatic arch, which corresponds to the level of the middle turbinate. A slow advance is made while the applicator is pushed laterally toward the back of the nasal pharynx. The ganglion lies a few millimeters beneath the lateral nasal mucosa. Once the first applicator is in place, a second applicator is inserted in the same fashion, except that it is placed slightly superior and posterior to the first. The applicators are left in for approximately 30 to 45 minutes. If additional medication is needed, the local anesthetic can be trickled down the shaft of the applicator. Because of the connections with the lacrimal gland,

Pterygopalatir ganglion {site ot block)

Pterygopalatir ganglion {site ot block)

Sphenopalatine Ganglion Block
Figure 40-2 Transnasal sphenopalatine ganglion block.

blockade of the SPG results in ipsilateral tearing because of unopposed parasympathetic activity. If the block is effective, it can be repeated, or an RFTC or EMF procedure can be performed for prolonged analgesia. I do not recommend the use of phenol for neurolysis with this technique.

Spencer ™ developed a variation of this approach at Concord Hospital in Concord, New Hampshire. Specific hollow-lumen, cotton-tipped applicators (Hardwood Products, Guilford, Me) are placed as described earlier. The white plastic disposable spray nozzle from a bottle of 10% Oral Spray (Astra, USA, Westborough, Mass) is cut to a length of 4 cm. A sterile 2.5-mm i.d. uncuffed tracheal tube is also cut to 4 cm and used to connect the spray nozzle to the hollow applicator. Each actuation of the metered-dose valve delivers 10 mg of lidocaine. The hollow lumen of the applicator is primed with two to three doses (not counted toward the total dose of lidocaine). Additional doses are administered and disconnected from the applicator. The applicators are left in place for at least 30 minutes. The applicators can be recharged with more local anesthetic during this time as long as the dose does not exceed 4 mg/kg.

TECHNIQUE TWO: GREATER PALATINE FORAMEN APPROACH ( Fig. 40-3 ) ™

The patient is placed in the supine position with the neck slightly extended. The greater palatine foramen is located just medial to the gumline of the third molar. Sometimes, a dimple can be seen, which signifies the foramen. A dental needle with a 120-degree angle is inserted through the mucosa and into the foramen. This procedure can be performed with or without fluoroscopic guidance. The needle is advanced approximately 2.5 cm in a superior and slightly posterior direction.

A paresthesia may be elicited because the maxillary nerve is just cephalad to the ganglion. If fluoroscopic guidance is used, 1 mL of a nonionic, water-soluble contrast is injected. The spread of the contrast into the pterygopalatine fossa should be visible. Cocaine or lidocaine, 2 mL, is injected after negative aspiration and the SPGB is confirmed as before. Data on standard radio frequency or electromagnetic field pulsed radio frequency lesioning, or phenol injection of the sphenopalatine ganglion via this approach appears to be absent from the literature.

TECHNIQUE THREE: INFRAZYGOMATIC ARCH APPROACH™

This approach has been commonly performed blindly without C-arm fluoroscopy, but at Texas Tech University Health Sciences Center, we recommend use of fluoroscopy. The patient is placed in a supine position with the head inside the C-arm. A lateral view of the upper cervical spine and the mandible is obtained. The patient's head is rotated until the rami of the mandible are superimposed. The C-arm is moved slightly cephalad until the pterygopalatine fossa is visible. When the 2 pterygopalatine plates are superimposed upon one another, they should resemble a vase and be located just posterior to the posterior aspect of the maxillary sinus (Fig. 40-4 (Figure Not Available) A). The needle is inserted under the zygoma and anterior to the ramus of the mandible. A curved, blunt-tip needle is less traumatic to the underlying structures than a sharp needle. When a blunt needle is used, a 1.25-inch angiocatheter needs to be inserted first. The needle is directed medial, cephalad, and slightly posterior toward the pterygopalatine fossa (see Fig. 40-4 (Figure Not Available) B). An anteroposterior view is obtained to confirm the direction and location of the needle (see Fig. 40-4 (Figure Not Available) C). The tip of the needle should be advanced until it is adjacent to the lateral nasal mucosa. If resistance is felt at any time, the procedure should be stopped and the needle redirected. One needs to be careful not to advance the needle through the lateral nasal

Lower Lip Regional Block
Figure 40-3 Greater palatine foramen approach.

mucosa. If a stimulating needle is used, sensory stimulation is performed on a I-V scale at 75 pulses per second and at a 0.25 to 0.5 millisecond pulse width.™ A paresthesia should be elicited at 0.5 to 0.7 V. When correctly situated on the ganglion, the paresthesia should be felt at the root of the nose. If the paresthesia is felt in the upper teeth, the maxillary branch of the trigeminal nerve is being stimulated, and the needle needs to be redirected in a more caudal and medial direction. Stimulation of the greater and lesser palatine nerves results in paresthesias of the hard palate. In this case, the needle is anterior and lateral, and should be redirected in a more posterior and medial direction. Once properly placed, 1 to 2 mL of local anesthetic with or without steroid is injected. If pain

Figure 40-4 (Figure Not Available) A, Lateral radiographic view of a 20-gauge curved, blunt needle in the pterygopalatine fossa. B, Anteroposterior view of the needle at the level of the middle turbinate. The tip is adjacent to the palatine bone. (Reprinted by permission of Blackwell Science, Inc.)

relief is obtained, RFTC or EMF pulsed radiofrequency lesioning can be planned.

TECHNIQUE FOUR: RADIOFREQUENCY THERMOCOAGULATION AND ELECTROMAGNETIC FIELD PULSED RADIO FREQUENCY LESIONING™

Lesioning of the sphenopalatine ganglion can be performed with either RFTC or EMF after a previous successful block with local anesthetic. The needle used is an insulated 20-gauge or 22-gauge, 10-cm, curved, blunt tipped SMK needle with a 5 to 10 mm active tip. After proper placement and stimulation as described in technique three, radiofrequency (RF) lesioning is performed for 70 to 90 seconds at 67°C to 80°C. Two lesions are usually made. Before lesioning, 1 to 2 mL of local anesthetic is injected. Electromagnetic field pulsed RF lesioning is performed at 42°C for 120 seconds. Two to three lesions (120 seconds) can be done without local anesthetic because the temperature of the lesioning is barely higher than normal body temperature.

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