Ultrasound-guided dry needling of masticatory muscles in trigeminal neuralgia – A case series of 35 patients

ABSTRACT

Background:

Trigeminal neuralgia (TGN) is considered a sensory neuropathy. However, reports of pain on chewing/speaking suggest a masticatory myofascial involvement.

Objective:

To examine the effect of ultrasound-guided dry needling (USGDN), which deactivates myofascial trigger points in masticatory, neck, and facial muscles on TGN symptoms.

Methods:

Charts of 35 patients treated for TGN were retrospectively reviewed. Treatment was USGDN alone or combined with trigeminal ganglion/mandibular nerve pulsed radiofrequency (PRF), followed by yoga mudras to stretch masticatory and facial muscles. Patients were followed for 1–8 years. Outcome parameters were reduction of medications with reduction in neuralgic attack frequency and Numeric Rating Scale (NRS) score.

Results:

23 patients (65.7%) received USGDN alone, 12 patients (34.3%) received PRF treatment before USGDN. A significant reduction in the mean (SD) NRS (5.7 [1.2] vs 8.8 [1.6]; P < .001) and neuralgic attack frequency (47 [27] vs 118 [70] attacks/day; P < .001) was seen after PRF compared with baseline, respectively. Following USGDN, the mean (SD) NRS further decreased significantly to 1.0 (0.9) (P < .001). USGDN alone produced a similar improvement in the NRS (8.9 [1.5] at baseline reduced to 0.6 [0.7] post-USGDN; P < .001). Patients in both groups reported a cessation in neuralgic attacks after USGDN. Post-USGDN, 18/27 patients completely discontinued medication, with the mean (SD) carbamazepine dose significantly reducing from 716.7 (260.9) mg/day at baseline to 113.0 (250.2) mg/day post-USGDN (P < .001).

Conclusion:

Decisive relief of TGN by USGDN suggests neuromyalgia involving masticatory muscles. Prospective, controlled studies could confirm these findings.

Introduction

Trigeminal neuralgia (TGN) is a condition that severely affects the quality of life.[1] Aging, multiple sclerosis, viral infection of the trigeminal ganglion, and compression of nerves by arterial or venous loops, meningiomas, and epidermoid cysts have been implicated in etiology.[2] Additionally, increased use of invasive dental procedures such as root canal surgery and dental implants has led to the emergence of a clinical entity called painful traumatic trigeminal neuropathy (PTTN).[3]

Medications form the first line of TGN therapy.[4] Interventional options, including percutaneous radiofrequency (RF) ablation, rhizotomy, and micro-vascular decompression, are considered only if medications are ineffective.[5,6] However, PTTN appears particularly resistant to standard pharmacological treatment.[7] Surgery for TGN has a higher success rate initially but has variable failure later with TGN recurrence.[8]

The current interventional procedures in pain management focus on ablation of the intra-cranial trigeminal ganglion, with the premise that relief of TGN pain justifies the use of a destructive procedure such as this. Over the past 16 years, we have developed safer treatments for TGN based on a novel concept that TGN manifests as neuro-myalgia involving both the trigeminal nerve and the masticatory muscles rather than being a pure neuralgia. The actual pain comes from myofascial trigger points (MTrPs) and taut bands in the masticatory muscles innervated by the mandibular division of trigeminal nerve. Only the mandibular division has a motor component and hence becomes the expressor for neuralgic involvement of the fifth nerve as neuromyalgia. This explains triggering of TGN pain by tongue movements, talking and chewing, which use masticatory muscles and the commonly observed trismus during TGN attacks. Anatomical and functional inter-connections between the trigeminal, facial, and cervical nerves 1–3 explain the involvement of the facial and neck muscles in TGN.[9] Based on this concept, we treat the neural component of neuro-myalgia with nerve preserving pulsed radiofrequency (PRF) of extra-cranial mandibular nerve and the myofascial component of neuro-myalgia by ultrasound-guided dry needling (USGDN) of masticatory, facial, and neck muscles. Dry needling has been reported to deactivate MTrPs and taut bands to relieve myofascial pain syndromes.[10,11,12,13,14] This includes two TGN cases and a meta-analysis of needling therapy in masticatory muscle pain.[15,16,17]

In this retrospective analysis of 35 patients, we examined whether TGN symptoms could be alleviated by USGDN as a sole treatment modality as well as in combination with mandibular nerve PRF.

Patients and Methods

The etiology, pain profile, and management of 35 TGN patients treated at Ashirvad Institute of Pain Management and Research are included in this study with 1–8 years of follow-up. The treatment protocol included medications [Table 1], PRF of the trigeminal ganglion/mandibular nerve, USGDN, and a novel yoga-mudra-based physiotherapy [Table 2 and Figures 1-5]. PRF was utilized to rapidly reduce the high neuralgic attack frequency in patients with severe frequent attacks.

Table 1.

Patient baseline Characteristics

Characteristics	All patients N =35	Ultrasound-guided dry needling (USGDN) only N =23	Pulsed radiofrequency (PRF) + USGDN N =12
Age in years, Range	30-65	30-65	35-65
Mean (SD)	54 (4.5)	60 (1.5)	49.2 (3.2)
Male	13 (37.1)	7 (33.3)	6 (42.9)
Female	22 (62.9)	14 (66.7)	8 (57.1)
Pain score on NRS (range)	5-10	5-10	5-10
Attacks per day (range)	6-300	6-60	60-300
Triggers on touch	30 (85.7)	18 (78.3)	12 (100.0)
Pain between attacks	30 (85.7)	19 (82.6)	11 (91.7)
V1 involvement	1 (2.8)	1 (4.3)	0
V2 involvement	4 (11.4)	3 (1.3)	1 (8.3)
V3 involvement	9 (25.7)	4 (17.4)	5 (41.7)
V1 + V2	1 (2.8)	1 (4.3)	0
V2 + V3	6 (17.1)	3 (13.0)	3 (25.0)
V1 + V2 + V3	14 (40.0)	11 (47.8)	3 (25.0)
Magnetic resonance imaging, MRI	21 (60.0)	13 (56.5)	8 (66.6)
Vascular loops present	11 (31.4)	7 (30.4)	4 (33.3)
Dental procedures*	24 (68.5)	14 (60.9)	11 (91.7)
Medications†
Carbamazepine family±	27 (77.1)	16 (69.6)	11 (91.7)
Pregabalin	11 (31.4)	5 (21.7)	6 (50.0)
Amitriptyline	7 (20.0)	3 (13.0)	4 (33.3)
Gabapentin	2 (5.7)	1 (4.3)	1 (8.3)
Clonazepam	1 (2.8)	0	1 (8.3)
Lioresol	1 (2.8)	1 (4.3)	0
Steroid injection	3 (8.6)	1 (4.3)	2 (10.0)
Tramadol + paracetamol	28 (80.0)	16 (69.6)	12 (100.0)
Diclofenac - oral/injections	6 (17.1)	4 (17.4)	2 (10.0)

Unless otherwise indicated, values are n (%); *includes root canals or extractions either before onset of pain, or to treat the pain; ^†some patients were receiving more than one medication; ± includes carbamazepine and oxcarbazepine; SD, standard deviation. V1, ophthalmic division; V2, maxillary division; and V3, mandibular division

Table 2.

Ultrasound-guided needle introduction into masticatory, facial, and neck muscles. Yoga mudras that target specific muscles

Muscle, its pain referral and innervation	Needle size and approach (es)	Notes on the technique of needle introduction
Medial pterygoids. Innervated by the undivided main trunk of mandibular nerve, refers pain to V2 and V3.	40-mm needles introduced via the mandibular notch directly perpendicular to the skin over the notch and advanced behind the maxilla and 25-mm needles introduced supero-medially at the mandibular angle, parallel to and just beneath the mandible. Figure 3 shows USGDN of both the pterygoids and masseter.	The needles via the mandibular notch go through the upper medial pterygoid to enter the lateral pterygoid. 25-mm needles from the mid-point of the sternomastoid can be seen to enter the lower part of the medial pterygoid as it lies deep to the hyperechoic mandible.
Lateral pterygoid innervated by the anterior division of mandibular nerve, refers pain to V2 and V 3 areas	40-mm needles introduced perpendicular to the skin through the mandibular notch toward the lateral pterygoid plate and 40-mm needles introduced from beneath the maxillary process of zygoma and passed laterally posterior to the ramus of the mandible to enter the masseter and lateral pterygoid muscles [Figure 3 and Row 1].	The superficial head of the masseter arising from the maxillary process of the zygoma can be visualized superficial to the lateral pterygoid as it passes laterally from the lateral pterygoid plate to insert into the pterygoid fossa and temporomandibular joint.
Masseter innervated by the anterior division of mandibular nerve, refers pain to V1, V2, and V3.	40-mm needles introduced in a medial to lateral direction from beneath the zygomatic process of the maxilla to enter the masseter before entering the lateral pterygoid. 25-mm needles introduced directly over the mandible.	Both heads of the masseter overlying the mandible can be visualized on ultrasound. The superficial head arising from maxillary process of the zygoma can be visualized superficial to the lateral pterygoid.
Yogamudras that stretch lateral and medial pterygoids and the masseter and temporalis muscles - Jihvabandha, simhamudra, khechari mudra, jaw thrust, and sideward jaw movements stretch both the pterygoids, masseter, and temporalis muscles. Jihva bandha (tongue lock) involves pushing up the tip of the tongue against the left of the hard palate as forcefully as possible. In simhamudra, the mouth is opened maximally, and the tongue protrudes as if it is being pulled out from its root to stretch all the masticatory muscles and facial muscles. Figure 4 shows many of the mudras.
Mylohyoids innervated by mandibular nerve posterior division	13-mm and 25-mm needles introduced perpendicular to the skin between the mandibular arch and hyoid to go through platysma to enter the mylohyoid muscle	Ultrasound determines the length of the needle to be used (13–25 mm) and to visualize the needle entering the platysma and the mylohyoid muscle.
Posterior digastric by facial nerve and anterior belly by nerve to mylohyoid. Both the digastric and mylohyoid refer pain to V3.	13-25-mm needles introduced perpendicularly beneath the digastric fossa at the chin into the anterior digastric belly. 13-25 mm needles introduced perpendicularly to the skin posterior to the mandible to enter the posterior digastric belly under vision.	The 13- or 25-mm needles can go through both the anterior belly digastric and mylohyoid under ultrasound visualization. The posterior belly lies close to the upper end of the sternocleidomastoid.
Yogamudras that stretch mylohyoid and digastric muscles - In khechari mudra, the tongue is rolled back on itself, and its underside pushes against the soft palate until muscles in the floor of the mouth beneath the rolled tongue can be felt to stretch. Smarana vardhak pranayama, jaw thrust, and sideward jaw movements stretch the platysma, neck muscles, lower facial muscles, masseter, and pterygoids.
Facial muscles innervated by facial nerve refer pain to all three areas of V1, V2, and V3.	13-mm needles introduced perpendicularly into frontalis, occipitalis, orbicularis oculi, procerus, nasalis, levator labii superioris alaeque nasi, levator labii superioris, orbicularis oris, buccinator, mentalis, and zygomaticofacial muscles.	These muscles are very superficial but can develop very painful spasms, particularly the orbicularis oris and oculi as well as the levator labii superioris alaeque nasi and platysma
Yogamudras that stretch facial muscles – Ballooning of the cheeks and lips to stretch the lower facial muscles and the buccinator. Smarana vardhak pranayama, where the lips are pouted and the head is extended backward on the neck along with a prolonged inhalation through the nose, with the head held in maximum extension for as long as it is comfortable. For exhalation, the neck is flexed fully, the mouth assumes a rictus pose where the teeth oppose each other, and a prolonged exhalation ensues through the teeth with a hissing sound. The neck automatically retracts at the end of the pose. Stretch is experienced in the platysma, neck muscles, lower facial muscles, particularly orbicularis oris, and the masseter during this practice.
Sternomastoid innervated by accessory nerve. Both its heads refer pain to V1, particularly to peri-orbital areas and V2 and V3 as well.	25-mm needles introduced in a medial to lateral approach into the sternocleidomastoid muscle visualized on ultrasound. These needles also address the platysma, [which refers pain to the V3 area] and the anterior scalene muscles. Needles targeting the medial pterygoid also pass through the sternomastoid.	Ultrasound should be used to safeguard the carotid artery and the internal jugular vein and visualize the needles passing from the sternomastoid to anterior and middle scalenes.
Posterior neck muscles innervated by C1-C3, refer pain particularly to V1 and V2, and V3 as well, as shown in Figure 6.	25-40-mm needles introduced perpendicularly into the trapezius, multifidus, semispinalis capitis and cervicis levator scapulae, splenius capitis, sub-occipital triangle muscles such as the rectus capitis posterior major, minor, superior and inferior oblique muscles. 40-50-mm needles passed from posterior to middle scalenes as well.	Ultrasound should be used to visualize the needles in these muscles. The vertebral artery pulsations help identify the sub-occipital triangle muscles such as the recti capitis major and minor and the inferior and superior oblique muscles for USGDN.
Neck muscles stretch with smaran vardhak pranayama and shadanana mudra, where the head is flexed, extended, turned, and bent on either side, with each pose being held for a duration of 5–10 slow deep breaths. Complete focus on breath has a calming effect on the anxiety and agitation because of pain.

Figure 1.

Mandibular nerve supply to the muscles targeted by USGDN. The main trunk supplies medial pterygoid and meninges before division. Anterior division innervates the temporalis, lateral pterygoid, masseter, and buccal nerve (sensory). The posterior division supplies mylohyoid, anterior digastric belly (posterior belly by facial nerve), auriculotemporal, inferior alveolar, and lingual nerves (sensory). (Image courtesy of Dr Rakhi More)

Figure 5.

Dry needling and relief of trismus in a patient. Left: mouth opening prior to needling. Center: placement of needles in masticatory and neck muscles. Right: Mouth opening increased from 2 cm at the baseline (left) to 5 cm (right) after one session of needling

Figure 2.

Surface markings of muscles for needling. Dots indicating needle entry points into probable myofascial trigger points in muscles of face (supplied by facial nerves), neck (spinal accessory, cervical 1–3 nerves), and masticatory muscles (motor root of trigeminal via mandibular nerve) targeted by ultrasound-guided dry needling

Figure 3.

Placement of the ultrasound probe (left) for showing needle placement (arrows) in the muscles during dry needling (right). First row: probe position for needling lateral pterygoids (LP). From cheek towards tragus. AAM - anterior aspect of mastoid. Second row: probe over the mandible (M) for needling superficial (SM) and deep masseters (DM). Third row: probe over the sternocleidomastoid (SCM). Fourth row: probe position for needling temporalis (T). N, needle; CA carotid; ant SC, anterior scalene

Trigeminal ganglion (TG) PRF: TG PRF was performed in six patients with pain in V1–V3 distribution with computerized tomography guidance. The patients lay supine with the head extended. A 22-gauge 10-cm insulated RF cannula with a 2.5-mm active tip (Cosman Medical, Burlington, VT) was directed superiorly and posteriorly through a skin wheal 2–3 cm lateral to the angle of mouth. A pilot shoot confirmed the needle direction. Later, axial sections delineated the anatomical structures clearly, making needle visualization and re-direction more accurate than fluoroscopy. Needle entrance into the foramen ovale was confirmed by a positive sensory response (at 50 Hz, 0.5–1.5 V) and the absence of a motor response (at 2 Hz, 0.1–1.5 V). PRF was carried out at 42°C for 8 minutes.

Ultrasound-guided mandibular nerve PRF: Ultrasound-guided mandibular nerve PRF was performed in six patients. A 10-cm 22-gauge RF cannula with a 2.5-mm active tip was introduced through the mandibular notch visualized between the coronoid and condylar processes. The lateral pterygoid plate was seen as a deep-seated shiny line. The RF needle was directed to the mandibular nerve near the alveolar artery to elicit sensory (pain paresthesia) and motor response with repetitive masseter twitches causing rhythmic up and down chin tap. PRF was then carried out at 42°C for 8 minutes, followed by injection of 10 mg of triamcinolone (Kenacort^®) and 2 mL of 0.125% bupivacaine.

USGDN: A linear 6–13 MHz probe of Sonosite™ MSK (Sonosite Inc., Bothell, WA) was used to guide the placement of 32-gauge 13-mm, 25-mm, 40-mm, or 50-mm needles into the masticatory muscles supplied by the mandibular division, facial muscles supplied by facial nerve and neck muscles supplied by the spinal accessory and the three cervical nerves as detailed in Table 2 and Figures 1–4. Individual needles were placed at 1-cm intervals longitudinally and horizontally across the surface marking of the muscle to be targeted. They were slowly advanced over a period of 2–3 minutes in 1-mm increments in facial muscles and 2–3-mm increments in the other muscles to make the needle passage comfortable to the patient. Needle removal after 30 minutes was followed by cold compresses to avoid possible bruising. USGDN was performed twice weekly until the patients reported about a 50–60% pain reduction from the baseline 10-point Numeric Rating Scale (NRS)[18] (usually within 2 weeks). Needling was reduced to weekly intervals thereafter. Once patients reported a decrease in NRS to 0–3, carbamazepine/other drugs were tapered by 100 mg/week until the lowest possible dose was reached, with USGDN continuing at fortnightly/monthly intervals before being discontinued.

Figure 4.

Poses of yoga mudras. Top row: Left: jihva bandha (tongue tie); center: simha mudra (lion pose); right: smaran vardhak pranayama (SVP) (inhalation). Middle row: Left and center: SVP (exhalation); right: khechari mudra. Bottom row: Left: sideway jaw movement; center and right: puffed-out cheeks and upper and lower lips

The patients were taught Yoga mudras with specific stretching effects on the masticatory, facial, and neck muscles [Table 2 Figure 4]. “Mudra” means a yoga pose that is held for at least a minute or more for optimal benefits. The patients performed them twice daily.

Outcome measures

The pain relief on NRS, the reduction in neuralgic attack frequency, and the carbamazepine dose were measured.

Statistical analysis

Data are represented as a range (minimum, maximum), percentages, or mean [standard deviation (SD)]. Between-group or pre- and post-treatment differences in the NRS score or carbamazepine dosage were analyzed using the paired t-test. P ≤ 0.05 was taken as the cut-off for statistical significance.

Results

Baseline patient characteristics are provided in Table 1. All 35 patients had sudden sharp intermittent pains {6–300 neuralgic attacks/day with NRS scores of 6–10 [mean (SD) = 8.9 (1.5)] in trigeminal distribution; Table 3}. A total of 21 of 35 patients had magnetic resonance imaging (MRI), and 11 had vascular loops (31%). A total of 24 patients (68%) had undergone dental procedures. Carbamazepine or its derivatives were the most prescribed anti-convulsant medication (27/35 patients: 77.1%), with a mean (SD) dose of 716.7 (260.9) mg/day. Other medications prescribed included pregabalin and amitriptyline [Table 1].

Table 3.

Pain relief after PRF and USGDN

Patient No.	Treatment included pulsed radiofrequency (PRF) and ultrasound-guided dry needling (USGDN)	Neuralgic attacks/day			Pain (NRS score)
		Base-line	Post-PRF	Post-USGDN	Base-line	Post-PRF	Post-USGDN
1	Trigeminal ganglion PRF + USGDN	60	40	0	10	4	1
2	Trigeminal ganglion PRF + USGDN	60	30	0	8	5	2
3	Trigeminal ganglion PRF + USGDN	100	60	0	7	5	1
4	Trigeminal ganglion PRF + USGDN	90	20	0	10	6	0
5	Trigeminal ganglion PRF + USGDN	100	30	0	8	5	2
6	Trigeminal ganglion PRF + USGDN	120	40	0	10	6	2
7	Mandibular nerve PRF + USGDN	300	100	0	10	6	0
8	Mandibular nerve PRF + USGDN	150	80	0	9	7	0
9	Mandibular nerve PRF + USGDN	200	80	0	8	8	2
10	Mandibular nerve PRF + USGDN	100	20	0	10	4	1
11	Mandibular nerve PRF + USGDN	60	20	0	5	6	0
12	Mandibular nerve PRF + USGDN	80	40	0	10	6	1
13	USGDN	6	N/A	0	10	N/A	1
14	USGDN	7	N/A	0	10	N/A	0
15	USGDN	8	N/A	0	5	N/A	2
16	USGDN	12	N/A	0	10	N/A	0
17	USGDN	8	N/A	0	8	N/A	0
18	USGDN	10	N/A	0	10	N/A	2
19	USGDN	8	N/A	0	7	N/A	1
20	USGDN	6	N/A	0	9	N/A	1
21	USGDN	12	N/A	0	6	N/A	0
22	USGDN	8	N/A	0	10	N/A	0
23	USGDN	14	N/A	0	9	N/A	1
24	USGDN	12	N/A	0	10	N/A	1
25	USGDN	60	N/A	0	10	N/A	0
26	USGDN	20	N/A	0	8	N/A	0
27	USGDN	10	N/A	0	10	N/A	1
28	USGDN	7	N/A	0	8	N/A	1
29	USGDN	40	N/A	0	10	N/A	1
30	USGDN	6	N/A	0	10	N/A	1
31	USGDN	10	N/A	0	10	N/A	0
32	USGDN	30	N/A	0	10	N/A	0
33	USGDN	20	N/A	0	7	N/A	1
34	USGDN	20	N/A	0	9	N/A	0
35	USGDN	24	N/A	0	9	N/A	0

N/A, not applicable; NRS, numeric rating scale

Patients reporting a high attack frequency (60–300 attacks/day; Table 3) received PRF treatment (n = 12), followed by USGDN, whereas those with a lower attack frequency (6–60 attacks/day) were treated with USGDN alone (n = 23). All patients were followed for a year after treatment completion. Eight patients have followed up with us for up to 8 years.

There were no major complications with USGDN. A few patients developed minor bruises, which resolved spontaneously. One TG PRF patient developed severe bradycardia, which was reversed uneventfully. One mandibular PRF had to be postponed because of hematoma because of bleeding from the pterygoid plexus, and the procedure was uneventfully performed on another day. One patient had a severe pain exacerbation for 2–3 weeks after mandibular PRF, but escalation of the carbamazepine dose (600 mg/day increased to 1600 mg/day), pregabalin (150 mg/day to 600 mg/day), and nortriptyline (from 10 mg/day to 25 mg/day) and USGDN (started 1 week after PRF), reduced pain to 0 NRS, and medications could be tapered.

A comparison of post-PRF versus baseline NRS scores showed a significant reduction in the mean (SD) NRS [5.7 (1.2) vs 8.8 (1.6); P <.001] and the mean (SD) neuralgic attack frequency [47 (27) vs 118 (70) attacks/day; P <.001]. However, patients needed to continue medication at baseline doses to maintain pain relief. After USGDN was initiated 1 week post PRF treatment, patients reported a further steady improvement in TGN symptoms. Within 10–12 sessions, a significant reduction in the mean (SD) NRS was observed when comparing post-USGDN with post-PRF treatment scores [1.0 (0.9) vs 5.7 (1.2); P <.001]. The USGDN-only group showed similar results, with patients reporting an almost complete reduction in the mean (SD) NRS post-USGDN compared with the baseline [0.6 (0.7) vs 8.9 (1.5); P <.001]. Patients in both groups reported a complete cessation of neuralgic attacks by the end of treatment [Table 3]. In both groups, within 7–12 sessions of USGDN, patients reported that they could start tapering medications. Of the 27 patients on carbamazepine or its derivatives, 20 patients (74.1%) discontinued the drug by the end of treatment. The post-treatment mean (SD) drug dose in the patients (n = 27) initially on carbamazepine or its derivatives was 113.0 (250.2) mg/day, significantly reduced from the baseline dose of 716.7 (260.9) mg/day (P <.001).

Spontaneous twitches in resting muscles were observable by ultrasonography in patients with severe TGN who presented with trismus (n = 12). One session of USGDN reduced the trismus [Figure 5] with significant reduction of TGN symptoms, accompanied by the disappearance of spontaneous twitches in resting muscles within 1–3 USGDN sessions.

Patients with severe pain were initially reluctant to perform yoga mudras, but the relaxation and pain reduction felt after the gentle slow performance of yoga mudras increased their compliance. In particular, the practice of Shadanana mudra produced a uniform reduction of pulse and blood pressure by about 10–15% (data not shown), and the patients reported that they felt a sense of calmness after this practice, which may have helped reduce the anxiety brought on by the frequent and painful neuralgic attacks. A total of 31/35 patients continued with the yoga mudras after treatment completion for sustained benefits.

Two patients (one in the mandibular PRF + USGDN group and the other in the USGDN-only group) had pain recurrence after 3 years and opted for surgery.

Discussion

This report is a retrospective analysis of our evolving understanding of the importance of USGDN in TGN. We initially followed the world view that treatment had to start with the ablation of the trigeminal ganglion where all three divisions converge to treat the pain in the designated V1, V2, and V3 facial areas. Instead of destructive thermal ablation, we preferred PRF followed by USGDN to prolong the PRF effect. As we treated more patients, we realized that patients were happier with USGDN, which appeared to be addressing their complaints with unequivocal reliability; although TG PRF reduced TGN frequency and pain intensity, it neither eliminated neuralgic attacks nor allowed medication reduction. However, USGDN predictably reduced the neuralgic attack frequency and pain intensity to 0 over 4–6 weeks, and medications could be reduced/discontinued over the next 4–6 weeks. Areas of pain referral from the neck, facial, and masticatory muscles as de lineated in the myofascial pain literature correspond to V1, V2, and V3[10] [Figure 6].

Figure 6.

Pain referral from head, face, and neck muscles. Row 1: Left: V1, V2, and V3. Right: Frontalis, trapezius, splenius cervicis, temporalis, trapezius masseter, and sternomastoid refer pain to V1. Row 2: Left: Masseter, temporalis, pterygoids, orbicularis oculi, zygomaticus, and sternomastoid refer pain to V2. Right: Sternomastoid, masseter, temporalis, pterygoids, trapezius, digastric, and platysma refer pain to V3. (Image courtesy Dr Mary Abraham MD based on reference 10)

USGDN of masticatory, facial, and neck muscles (especially sternocleidomastoid and splenius) effectively, consistently, and always predictably relieved the V1 pains, particularly peri-orbital and eyeball pain. Similarly, V2 area pain responded to USGDN of the underlying masseter, temporalis, pterygoids, and facial muscles, indicating that these were the TGN pain generators. The V3 area appeared to be the referral zone for platysma, neck, facial, and masticatory muscles. Thus, when muscles were considered as the cause of TGN pain, the motor root assumed importance as the target of neural interventions; more importantly, it addressed the pain attributed to V1 and V2 as well. The risky interventions on the intra-cranial trigeminal ganglion could be replaced with the safer PRF of extra-cranial mandibular nerves. In this study, the mandibular PRF and USGDN combination ensured TGN remission in severe cases enabling medication cessation/reduction, whereas milder presentations responded to USGDN alone.

These findings call for a revaluation of the mechanisms underlying TGN. Current TGN treatments neither acknowledge nor address the myofascial mechanism of pain in TGN. The current understanding attributes TGN to demyelination with hyper activity secondary to vascular compression of trigeminal rootlets at the pons.[19,20,21] However, the RF procedure that targets the trigeminal ganglion and leaves the rootlet compression untreated, is the presently accepted interventional pain management treatment of TGN.

Our findings in this patient cohort suggest that the motor root and the muscles it innervates plays as important a role in TGN etiopathogenesis as the sensory fibers. The motor root as it emerges from the side of the pons is equally susceptible to compression by superior cerebellar arteries and vulnerable to demyelination.[21] The well-established ignition hypothesis of TGN could apply to motor nerves as well, causing spontaneous repetitive electrical discharges.[22,23]

Saunders et al.[24] reported a higher incidence of pain recurrence after neurectomy when motor rootlets were spared. Additionally, Ongerboer et al.[25] reported two cases of TGN relapse after surgery because of motor rootlet issues. They proposed that in TGN, motor or sensory disorders can supplement each other or occur separately.

Trigeminal nerve branches are also vulnerable to entrapment at sharp bends in their course and compression between the muscles they innervate and the unyielding surface of the skull or mandible [Figure 1]. In particular, the main trunk of mandibular nervescould be entrapped as it traverses between two heads of the lateral pterygoid muscle, similar to sciatic nerve compression between piriformis and gemelli muscles.[26] Focal de myelination of entrapped nerves could lead to ectopic activity inherent to TGN, resulting in MTrP formation in masticatory muscles. MTrPs may be initially painless (latent MTrPs) but progress to being active MTrPs which are spontaneously painful. In addition, shortening of masticatory muscle fibers into taut bands results in pain on their movements during chewing, biting, speaking, etc., Sudden contraction of these bands could be felt as the shocks of TGN. Frank trismus from extreme spasm of mouth closers was seen in 12 of our patients, whereas other patients had difficulty in mouth opening and speech during attacks.

We surmise that vascular compression of motor rootlets might be ‘dynamic’ in that the vessels compress the rootlets intermittently during certain movements, rather than a constant compression. Intermittent firing at the neuromuscular junction of masticatory muscles probably leads to MTrP generation, taut bands, nerve entrapments, etc., which can worsen with stressful life situations or excessive use of masticatory muscles as in bruxism. When MTrP numbers reach a critical level, TGN manifests. Increased traffic in free nerve endings in muscles that convey nociceptive signals from the MTrPs (musculo-sensory afferents) to the CNS could lead to the development of central sensitization. All this explains how a peripheral treatment such as USGDN of masticatory muscles relieved the pain in patients with vascular compression of nerve roots on MRI (n11).

Real-time observation of muscle events at rest showed that TGN shocks correspond with sudden sharp twitches in muscles observable on ultrasound Video 3. Severe constant pain and trismus are associated with flickers in the resting masseter, temporalis, and pterygoids (Video 2). Ultrasound visualization during USGDN shows that needle introduction elicits local twitch reflex (LTR) Video 1. When the needles have remained in situ for a few minutes, the muscle twitches associated with shocks and pains subside, corresponding to perceptible relief of the patient's own pre-needling pain. Thus, ultrasound objectively ‘demonstrates’ TGN pain and its relief by USGDN. The post-USGDN pain relief is reflected as quiescence in the resting muscle at the next session and easier needle introduction through muscles that feel 'softer’ to the advancing needle. Observations from our patients who return with a pain recurrence after years of remission reveal that their lateral pterygoids have become tight and offer extreme resistance to needle passage. Two to three sessions of USGDN relieve this tightness, and needle passage becomes easy and painless with accompanying TGN relief. This tight Lateral Pteryaoid presumably causes mandibular nerve entrapment. Cumulative reduction of pain, stiffness, and weakness over successive USGDN sessions along with specific stretches of yoga mudras translated into a complete reversal of pain in TGN in our patients.

The MTrP literature describes that electromyography of the normal neuromuscular junction shows spontaneous electrical potentials at approximately 6/second called miniature end plate potentials (MEPPs), whereas MTrPs show a barrage of potentials (110 per second) called end plate noise (EPN) because of the grossly (3×) increased release of acetylcholine from the nerve terminal.[10,11] The EPN is associated with painful muscle contracture, which is reduced by dry needling.[27,28,29] Histopathology of human MTrPs has also shown abnormally contracted sarcomeres.[30]

Collectively, these findings suggest that although the compression along the trigeminal rootlets by arterial or venous loops, multiple sclerosis, persistent viral infection of the trigeminal ganglion, and nerve entrapment or PTTN initiates the process of neural de myelination with spontaneous repetitive electrical discharges in motor nerves, it appears to be the consequent MTrP formation in taut bands that cause the shocks of TGN. Once formed, MTrPs become independent of the original neural irritation that caused them in the first place and sustain TGN. Unrelieved MTrPs in masticatory, facial, and neck muscles can persist and maintain the central and peripheral sensitization long after surgical de compression of rootlets definitive or trigeminal ganglion ablation, explaining the failure of these procedures in some patients.

Our patient cohort with varying etiology (31% with vascular compression and 68% with dental procedures) had a common finding of painful MTrPs in the masticatory, facial (particularly orbicularis oculi and oris), and neck muscles. USGDN proved to be a specific treatment for MTrPs, which appeared to be the direct cause of TGN pain, even though they might have been the effect of rootlet compression at the pons or of the mandibular nerve by lateral pterygoids. The success of USGDN with complete alleviation of TGN symptoms indicates the dominance of the myalgia component in this cohort. Presumably, USGDN not only inactivated MTrPs but also reduced the central sensitization because of painful MTrPs.

Mandibular PRF, USGDN, and yoga mudras are new treatment modalities which do not figure in contemporary treatments of TGN. However, unequivocal remissions lasting for years with little or no medication support, the predictable response of recurrences to repeat treatment, and patient empowerment by the ability to live normally give credence to the concept of neuromyopathy. Our previous studies have shown that several neuropathic pains are in fact neuromyopathic, with muscle pathology that responds to USGDN.[31,32,33,34,35,36,37,38,39,40,41,42,43,44]

To summarize, this publication highlights for the first time that TGN may be a neuromyalgia that can be addressed specifically by USGDN and customized physiotherapy with sophisticated yoga mudras along with the judicious addition of mandibular nerve PRF in select patients. Mandibular nerve PRF is much safer than the currently practiced ablative procedures of the trigeminal ganglion. USGDN is minimally invasive and safe. However, USGDN for TGN can only be performed by skilled pain specialists with a thorough understanding of the 3D anatomy of the intricate head and neck musculature and who have acquired sonoanatomical capability to safeguard vital structures during USGDN. The limitations are the retrospective study design and the lack of a control group. Prospective randomized controlled studies comparing the effect of PRF with that of USGDN in large patient cohorts would determine the clinical value of USGDN in treating TGN. Yoga mudras need further investigation as an independent modality.

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Conflicts of interest

There are no conflicts of interest.