Interventional Procedures for Facial Pain

Anesthetic Techniques in Pain Management (KA Williams, Section Editor)
Part of the following topical collections:
  1. Topical Collection on Anesthetic Techniques in Pain Management


Interventional pain procedures are critical in the diagnosis and management of a variety of facial pain conditions. Trigeminal neuralgia (TN) is the most frequent diagnosis for facial pain, with a reported prevalence 10 times greater than persistent idiopathic facial pain (PIFP). Although pharmacological treatments and psychological interventions benefit many patients with these diagnoses, the pain remains disabling for a significant portion of others. Percutaneous interventions targeting the gasserian ganglion and its branches have proven effective in the management of TN, while there is also supportive evidence for treating the sphenopalatine ganglion in PIFP.


Facial pain Interventional techniques Trigeminal neuralgia Tic douloureux Persistent idiopathic facial pain Atypical facial pain Radiofrequency ablation Trigeminal (Gasserian) ganglion Sphenopalatine (pterygopalatine) ganglion Mandibular nerve Maxillary nerve Neuromodulation Peripheral nerve stimulation 


Chronic facial pain may result from a diverse assortment of causes including trauma, structural abnormalities (temporomandibular joint), infections, tumors, central nervous system (CNS) diseases, vascular abnormalities, and nerve compression; or it may reflect referred pain from the face or neck. The trigeminal nerve, cranial nerve five (CN V), is involved in the vast majority of cases and pain most commonly affects the maxillary (V2) and/or mandibular (V3) branches. Although TN and PIFP are 2 of the most common etiologies, other “red flag” conditions (tumor, infection, vascular abnormality/dissection, fracture, and intracranial hemorrhage) must first be excluded. In addition, other comorbidities, such as demyelinating, autoimmune, or neuromuscular conditions, should be identified. This article will focus on the clinical characteristics and anatomy relevant to TN and PIFP and the interventional techniques for patients with these conditions.

Trigeminal Neuralgia

Trigeminal neuralgia, although the most common form of facial neuropathic pain in the elderly, is a rare neurological disorder, with an estimated 15,000 new cases per year in the United States [1•]. Worldwide incidence of new patients is commonly reported in the range of 4–5/100,000 (0.004 %) [2]; however, a recent population based study of 3336 people in Essen, Germany found a lifetime prevalence nearly one-hundred-times greater than the prior estimates (10/3336, 0.3 %) [3]. The same study found that TN had a 10-times greater lifetime prevalence than PIFP in the same population (1/3336, 0.03 %). Trigeminal neuralgia is more common in women (1.5:1) and the elderly, with a peak age between 50–80 years (most common in the seventh decade of life). The etiology is often due to vascular compression of the nerve at the brainstem or distally. There are 2 types of TN with identical clinical features: (1) classical TN (Table 1) and (2) symptomatic TN (if a structural lesion other than vascular compression is identified as etiology).
Table 1

ICHD-II diagnostic criteria for classic TN [4]


Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting 1 or more divisions of the trigeminal nerve and fulfilling criteria B and C


Pain has at least 1 of the following characteristics:

1. Intense, sharp, superficial, or stabbing

2. Precipitated from trigger areas or by trigger factors


Attacks are stereotyped in the individual patient


No clinically evident neurologic deficit


Not attributed to another disorder

ICHD international classification of headache disorder

The symptoms of both types of TN consist of pain in 1 or more branches of the trigeminal nerve (Table 2). The pain rarely occurs bilaterally and more commonly affects the right side (59 % to 66 %). If the pain is bilateral, a central cause such as multiple sclerosis (MS) should be considered. Between paroxysms, the patient is usually pain-free, but a dull, continuous pain may persist in some long-standing cases, suggesting a role for central sensitization [5]. A painful paroxysm is often triggered by non-noxious stimuli (touch, movement, wind exposure, brushing teeth, shaving, chewing, and swallowing) and is usually followed by a refractory period during which pain cannot be triggered. Such triggers are often on the anterior aspect of the face, especially the nasolabial fold and the side of the chin. The pain frequently evokes spasm of the muscle of the face on the affected side (tic douloureux).
Table 2

Pain distribution in the various nerve branches in trigeminal neuralgia

Trigeminal nerve branch affected (pain)

Percentage (%) of patients

V1 only


V2 only


V3 only


V1 + V2


V2 + V3


V1 + V2 + V3


Modified and used from [1•], with permission

Findings on neurologic examination are essentially normal in patients with classic TN, although abnormalities are noted with blink reflex (BR), and quantitative sensory testing (QST) commonly reveals thermal hypoesthesia [6]. Gross abnormalities on neurologic examination are more indicative of symptomatic TN. Magnetic resonance imaging (MRI) is essential to identify any neurovascular compression and to rule out other pathology, such as MS, or posterior fossa tumors (symptomatic TN). Although the presence of vascular compression on MRI may determine subsequent treatment approaches, it is worthwhile to note that compressing blood vessels are seen in one-third of asymptomatic patients [7].

Persistent Idiopathic Facial Pain

Persistent Idiopathic Facial Pain (PIFP), previously termed “atypical facial pain”, is described as a persistent facial pain that does not have the classical characteristics of cranial neuralgias and for which there is no obvious cause (Table 3) [4]. Although the estimated incidence has been (under-) reported as 1/100,000 [9], Mueller showed 1/3336 in their study [3]. The diagnosis is made following exclusion of other possible causes and if pain is present daily (for all or most of the day), and is fairly localized. Pain is usually in the maxilla, but may extend to the eyes, nose, cheeks, and temple. By definition, neurological and physical examination findings should be normal; however, abnormalities are often appreciated on more sensitive tests, including QST and BR assessments [6].
Table 3

ICHD-II diagnostic criteria for PIFP [4]


Pain in the face, present on a daily basis, satisfying criteria B and C


Pain is confined at onset to a limited area on one side of the face, is deep and poorly localized


Pain is not associated with sensory loss or other physical signs


Clinical and imaging investigations do note demonstrate any relevant abnormalities of the face

ICHD international classification of headache disorder.

In addition, particular attention to ruling out metastatic lung cancer is noted, as well as other differential diagnoses, including cervicogenic headache. Table 4 illustrates some of the differences between the characteristics of TN and PIFP. Compared with TN, patients with PIFP benefit less from medications, interventional procedures; and open surgical techniques.
Table 4

Clinical features of trigeminal neuralgia and persistent idiopathic facial pain


Trigeminal neuralgia (Tn)

Persistent idiopathic facial pain (Pifp)/atypical facial pain

Age of onset (y)



Gender (female:male)





Constant, fluctuates

Pain-free intervals


Rarely, never


Electric, stabbing, shooting

Burning, aching

Precipitation factors

Triggered, non-noxious

Rarely triggered

Causative factors

Vascular, multiple sclerosis, tumor

Idiopathic, tumor, Infection, trauma, Mechanical

Normal BR and QST*

0 %

25 %

Abnormal QST*

 -Thermal hypoesthesia

100 %

45 %

 -Warm allodynia


10 %

BR changes*

 -Abnormal BR

58 %

15 %

 -Deficient habituation (excitability)

33 %

35 %

* BR Blink Reflex; QST Quantitative Sensory Testing

Data from Forsell et al. [6]

Although there is often overlap between the signs and symptoms of these 2 conditions, a series of 6 questions has been proposed to differentiate between these 2 causes and other types of orofacial pain [8]. These include:
  1. A.

    Does the pain occur in attacks?

  2. B.

    Are most of the attacks of a short duration (seconds to minutes?)

  3. C.

    Do you sometimes have extremely short attacks?

  4. D.

    Are the attacks unilateral?

  5. E.

    Do the attacks occur in the distribution of the trigeminal nerve?


Treatment of Orofacial Pain

Conservative Care

Pharmacologic therapy with antiepileptic drugs (AEDs) is often effective, at least initially in patients with classic TN. Carbamazepine (alternatively, oxcarbazepine) is considered first-line therapy, although the addition of baclofen and/or lamotrigine may be of increased benefit [10]. These medications appear less effective in patient with PIFP; however, often a trial of amitriptyline, venlafaxine, fluoxetine, or antiepileptic drugs (AEDs) is indicated [8, 11•]. Transcutaneous electric nerve stimulation (TENS) and orthodontic care has also demonstrated benefit for patients with kinesiology (CMS) and electromyography (EMG) verified abnormal facial muscle tone at rest leading the author to conclude: “All patients with PIFP should undergo the CMS-EMG exam [9].”

Psychological treatment is important for patients with orofacial pain. Up to 30 % of these patients may have anxiety disorder and PIFP is associated with multiple psychiatric comorbidities [12]. Remich and Blasberg reported 68 % of patients with PIFP having various psychiatric disorders, including: affective, somatoform, and psychosis [13]. A recent study of patients with PIFP reported regional differences in gray matter density/volume in several areas, including the ipsilateral anterior cingulate gyrus (ACG) and insular cortex [14]. These areas are known to play a critical role in antinociception and anticipation of pain experience for a variety of pain experiences [15]. This study also found thinning in somatosensory and motor cortex, believed to be areas specific to face pain. Similar models have been described for trigeminal neuralgia [16]. It is still not entirely clear whether these changes are a result of the underlying pain condition vs a predisposing factor for the development, but these studies demonstrate reproducible altered brain morphology in patients with chronic facial pain.

If conservative measures are ineffective or not tolerated, early referral for interventional therapies is appropriate. Surgical management of TN may be broken down into open surgical methods and minimally invasive methods. All of the interventions appear to be most successful for patients whose symptoms are typical of their condition and conform to the diagnostic criteria. The decision on which technique to utilize depends on the patient’s age and comorbidities, anatomy, and etiology of pain condition and the physician’s clinical experience.

Anatomy of the Trigeminal (Gasserian) Ganglion and Trigeminal Nerves

The trigeminal nerve or fifth cranial nerve (CN V) is the largest among the facial nerves and its branches provide the cutaneous innervation of the head and face. It also innervates muscles that move the lower jaw. The trigeminal (Gasserian) ganglion, located in the middle cranial fossa, was named after Johann Lorentz Gasser (1723-1765), a Viennese anatomist [17]. The ganglion occupies a cerebrospinal fluid (CSF) containing cavity (Meckel’s cave) in the dura mater, with the dura covering the posterior two-thirds of the ganglion. The ganglion, formed by the fusion of a series of mid-pontine rootlets, is located near the apex of the petrous part of the temporal bone. The ganglion is bound medially by the cavernous sinus and optic and trochlear nerves; superiorly by the temporal lobe and posteriorly by the brain stem. The ganglion interfaces with the autonomic nervous system through several ganglia and also communicating nerves. These include the ciliary, sphenopalatine, otic and submaxillary ganglia, and the oculomotor, facial, and glossopharyngeal nerves. The trigeminal ganglion has 3 major divisions: ophthalmic (V1), maxillary (V2), and mandibular (V3). These are located dorsally, intermediate, and ventrally within the middle cranial fossa, respectively.

The ophthalmic division (V1), upon exiting the ganglion, passes into the orbit via the superior orbital fissure. This course makes the V1 division a poor target for blockade once it leaves the ganglion. V1 branches into the supraorbital, supratrochlear, and nasociliary nerves which provide sensory innervation from the forehead and nose. The maxillary division (V2) exits the middle cranial fossa via the foramen rotundum. It then crosses the pterygopalatine fossa, making it amenable to percutaneous approaches, before entering the orbit through the inferior orbital fissure. The infraorbital, superior alveolar, palatine, and zygomatic nerves, all arising from V2, carry sensory information from the maxilla and overlying skin, nasal cavity, palate, nasopharynx, and meninges of the anterior and middle cranial fossa. The mandibular division (V3) exits the middle cranial fossa via the foramen ovale prior to dividing into the buccal, lingual, inferior alveolar and auriculotemporal nerves. In addition to the sensory input from these nerves, the motor component of V3 innervates the muscles of mastication, tensor tympani, tensor vili palatine, myelohyoid, and anterior belly of the digastric. Most of the lower face (including chin, teeth, gums, and anterior two-thirds of tongue) sensory input is communicated via the mandibular division, with the exception of a small area covering the angle and lower body of the ramus of the mandible and parts of the ear, all of which are innervated by cervical nerves.

Interventional Techniques

Where to Target?

The decision of what interventional strategy to utilize depends on the patient’s pain distribution, pain characteristics, comorbidities, and operator experience. Blockade of the terminal branches may be an initial starting point if the patient has isolated pain in 1 or 2 nerve distributions. These branches include the supraorbital and supratrochlear nerves (ophthalmic division, V1), infraorbital nerve (maxillary division, V2), and mental nerve (maxillary division, V3). If the pain is isolated to 1 division, maxillary, and/or mandibular, then a targeted block of V2 and/or V3 may be indicated. Due to its course of exit from the trigeminal ganglion into the orbit, a peripheral block of the V1 division is not possible. Therefore, generally if the patient has pain in the V1 division or in more than 1 other division, interventional strategies targeting the Gasserian (trigeminal) ganglion may be indicated. It should be noted that although blockade of the terminal branches or divisions may be helpful for diagnostic purposes, there are limited studies showing sustained benefit from blockade or neurolytic procedures targeting these structures. Conversely, there is demonstrated benefit with approaches targeting the trigeminal or sphenopalatine ganglion.

Percutaneous Trigeminal (Gasserian) Ganglion and Nerve Treatments

A percutaneous transovale approach to the trigeminal (Gasserian) ganglion for ethanol neurolysis was first published by Hartel in 1912 [18]. Since that time, glycerol, first described by Hakanson in 1981 [19], has demonstrated more benefit than ethanol for injection and therefore ethanol injection has largely been abandoned. An alternative percutaneous procedure targeting the trigeminal ganglion is balloon compression, first described by Mullan and Lichton in 1978 and first published in 1983 [20].

Radiofrequency ablation (RFA) of the Gasserian ganglion was first described as a successful treatment for TN by Dr. Sweet in 1965 [18] and published in1974 [21]. Numerous other studies have demonstrated similar efficacy (80 %–98 % high-grade or complete relief) [1•, 17, 22, 23, 24]. A 15 %–20 % symptom recurrence rate can be expected within the first year, and 4 %–65 % in studies that track patients up to 13 years. RFA demonstrated better initial success rate and less likelihood of symptom recurrence at 1 year compared with other percutaneous techniques [23, 24]. Kanpolat et al [23]in their series of 1600 patients who underwent trigeminal ganglion RFA for TN, reported acute pain relief in 97 % of patients, although that fell to 92 % at 1 year. At 10 and 20 years, the relief rate from the single procedure was 52 % and 42 %, respectively. However, those patients who underwent multiple procedures had reported pain relief of 94 % and 100 % at 10 and 20 years after initial treatment. Wu et al [25] demonstrated similar benefit in their series of 1860 patients.

Technique of Trigeminal Ganglion RFA

Prior to RFA, the patient should have at least 1 diagnostic block. The technique for blockade of the trigeminal ganglion is identical to that for RFA except that 1 mL of local anesthetic is injected once motor stimulation is elicited (and after live contrast injection demonstrates lack of intravascular spread). Complete or significant (>50 %) relief is expected prior to proceeding to RFA.

The patient should have an intravenous line established and often requires sedation. The patient is placed supine with his head within the C-arm. The c-arm is rotated into an ipsilateral oblique, submental view to optimize visualization of the foramen ovale which often projects medially to the mandibular process. After injecting local anesthetic over this area (typically 2 cm lateral to the corner of the mouth), a 22 G, 10 cm RFA cannula is advanced towards the foramen ovale under real-time fluoroscopy in the AP submental and then lateral view. A finger should be placed into the oral cavity to prevent and detect oral mucosa penetration. After the needle is inside the foramen ovale (Fig. 1), motor stimulation should result in muscle twitches of the mastication muscles (V3). If treatment of the V2 or V1 branches is desired, then the needle should be advanced deeper (∼2 mm) until the needle tip is visualized over the petrous bone. Then sensory stimulation at 50Hz should be felt in the painful areas at 0.05–0.1 V. Once appropriate stimulation is attained, and after negative aspiration for heme and CSF, 0.5–1 mL of contrast should be injected under real time fluoroscopy, with digital subtraction angiography (DSA) if possible, to rule out intravascular spread. If CSF is aspirated, the needle should be repositioned and the practitioner should consider the administration of broad spectrum antibiotics. Then, 1–2 ml of lidocaine or bupivacaine +/- non-particulate corticosteroid (dexamethasone 10 mg) may be injected prior to lesioning. The first lesion is performed at 60 degrees for 60 seconds and then a second (or even third) lesion is performed for an additional 60–120 seconds at 60–70 degrees.
Fig. 1

Gasserian (trigeminal) ganglion RFA: a, Oblique, submental view showing the needle tip approaching inferior to the foramen ovale. b, Lateral image demonstrating further needle advancement into the foramen ovale.

The main anticipated side effect following RFA of the trigeminal ganglion is sensory loss in the distribution of the treated nerve(s), but may also involve corneal anesthesia, and masseter weakness. Adverse events related to needle placement for block or RFA lesioning include cheek or retrobulbar hematoma (with exophthalmos), keratitis, meningitis, transient rhinorrhea, intravascular injection, and dural arteriovenous fistulae. Other potential complications related to RFA lesioning include anesthesia dolorasa and hypoesthesia. Anesthesia dolorosa, deafferentiation pain, is less common (1 %–5 %) but can be quite severe and disabling. There have been reports of intracranial hemorrhage, stroke, and death following trigeminal ganglion RFA [17, 26, 27].

In theory, pulsed radiofrequency (PRF) of the Gasserian ganglion may avoid some of these side effects because it is a neuromodulatory rather than neurodestructive procedure [28]. This technique would be expected to have minimal sensory or motor loss, anesthesia dolorosa, and potentially even fewer corneal abnormalities. Unfortunately, in clinical practice the procedure has shown mixed results in terms of efficacy. Van Zundert et al [29] reported excellent long-term relief (19 month mean follow-up) in 3/5 patients with partial relief in 1 patient and short-term effect in the other. In contrast, Erdine et al [30] showed minimal relief with PRF compared with RFA of the Gasserian ganglion, although it should be noted that the authors’ reported success with (conventional) RFA was far below the efficacy reported in other studies. At this time there is not enough supporting evidence to recommend PRF over RFA of the Gasserian ganglion.

Extracranial peripheral nerve denervation may be considered for patients with more localized pain. This may be performed at the supraorbital notch (V1), infraorbital notch (V2), and the mental foramen (V3). Alternatively, the maxillary (V2) and mandibular (V3) divisions may be blocked more proximally at either the foramen ovale or after first contacting the lateral pterygoid plate via the infrazygomatic approach under fluoroscopic [22] or CT [31] guidance. There are case reports of patients with TN benefitting from pulsed RF (PRF) treatment to the mental nerve [32] and also V2 PRF combined with topical SPG block and oral medications [33]. Greater occipital nerve blockade with local anesthetic and corticosteroid has also been reported to benefit patients with TN [1•], but is less beneficial in patients with PIFP [34].

Sphenopalatine (Pterygopalatine) Ganglion Radiofrequency Treatments

Blockade of the sphenopalatine ganglion (SPG), also known as the pterygopalatine ganglion (PPG), can be most reliably accomplished via an infrazygomatic approach under fluoroscopic guidance, Although “blockade” is often performed via trans-nasal application of local anesthetic (LA) soaked cotton-tipped applicators, this relies upon diffusion (both trans-mucosal and trans-bony) of the LA and is unpredictable [35••]. Similarly, intra-oral injection of LA via the greater palatine foramen is a “blind” technique that does not allow verification that the LA injectate has actually reached the SPG [36]. Please see Dr. Narouze’s excellent description in a prior issue of this journal [37••] on the neuroanatomy of the SPG and technique of SPG-RFA.

Radiofrequency ablation (RFA) and pulsed radiofrequency (PRF) of the sphenopalatine ganglion has demonstrated benefit for cluster headache [35••, 37••, 38], but no controlled studies have been published for PIFP. A retrospective study of PRF of the SPG (PRF-SPG) for 30 patients with chronic facial pain (including “atypical facial pain”) demonstrated complete relief in 21 % and 65 % experienced good or moderate improvement [39]. Similarly, Varghese [40] reported early relief in 77 % of patients undergoing SPG ablation with 6 % phenol via a nasal endoscopy guided approach for facial pain due to head and neck cancers. Neither SPG neurectomy [41] nor radiosurgery [42] provided sustained benefit for patients with PIFP.

Side-effects and complications of RFA-SPG are directly related to the close proximity of other nerves and vasculature. Persistent anesthesia, hypoesthesia, or dysesthesia of the palate, maxilla, or posterior pharynx often occurs. Dryness of the eye, typically temporary, is common due to interruption of the parasympathetic supply. The most common complication is cheek hematoma which may occur after puncturing the maxillary artery which lies in the pterygopalatine fossa. Intravascular injection, epistaxis (if needle is advanced through lateral nasal wall), and infection (particularly if the oral or nasal mucosa are penetrated) are other potential sequellae. Profound reflex bradycardia has been reported during RFA-SPG, likely related to the rich parasympathetic connections to the SPG.


Neuromodulation, namely peripheral nerve stimulation of the supratrochlear, supraorbital, infraorbital, and occipital nerves has shown promise for patients with trigeminal autonomic cephalgias, including cluster headache [43] and other causes of refractory craniofacial pain [44]. Peripheral nerve stimulation is a promising technique for investigation in patients with TN and PIFP.

Open Surgical Approaches

Microvascular decompression has demonstrated benefit in patients with persistent TN due to vascular compression of the nerve. The vessels in contact with the nerve are coagulated or separated from the nerve using an inert sponge. This approach is often indicated for younger patients without significant comorbidities who have clear evidence of vascular compression [22]. Although the recurrence rate appears lowest with this technique, microvascular decompression is not considered first-line therapy for TN as it involves the morbidity associated with a suboccipital craniotomy. Other techniques, such as gamma-knife surgery, have also demonstrated good benefit for patients and potentially with less comorbidity than MVD. A detailed discussion of these and other neurosurgical techniques have been previously reviewed [45•] and are beyond the scope of this article.


When facial pain persists following conservative treatment, a number of interventional procedures may be considered. In particular for patients with trigeminal neuralgia, trigeminal ganglion RFA has well documented efficacy over the past 4 decades that appears superior to other percutaneous approaches. For younger patients with verified vascular compression, microvascular decompression may demonstrate similar efficacy with an even lower recurrence rate following a single treatment. The majority of patients with persistent idiopathic facial pain have coexisting psychiatric conditions that should be treated, although RFA of the sphenopalatine ganglion remains a promising treatment when symptoms remain bothersome. Emerging treatments, including PRF of trigeminal divisions and peripheral nerve stimulation, offer potential techniques for future investigation.



No potential conflict of interest relevant to this article was reported.


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Copyright information

© Springer Science+Business Media New York 2012

Authors and Affiliations

  1. 1.Department of Anesthesiology & Pain MedicineVirginia Mason Medical CenterSeattleUSA

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