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Ultrasound-guided dry needling of masticatory muscles in trigeminal neuralgia – A case series of 35 patients L Vas, S Phanse, KS Pawar, R Pai, M PattnaikAshirvad Institute for Pain Management and Research, Mumbai, Maharashtra, India
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/jpgm.jpgm_797_21
Keywords: Neuromyalgia, neuromyopathy, pulsed radiofrequency, trigeminal neuralgia, ultrasound-guided dry needling
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.
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 [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]. PRF was utilized to rapidly reduce the high neuralgic attack frequency in patients with severe frequent attacks.
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 [Figure 1], [Figure 2], [Figure 3], [Figure 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. 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.
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].
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.
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].
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 [Additional file 1]. Severe constant pain and trismus are associated with flickers in the resting masseter, temporalis, and pterygoids (Video 2 [Additional file 2]). Ultrasound visualization during USGDN shows that needle introduction elicits local twitch reflex (LTR) Video 1 [Additional file 3]. 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. Acknowledgements The authors are grateful to Dr. Rakhi More [for [Figure 1]] and Dr Mary Abraham [for [Figure 6]] for their assistance in rendering the anatomical diagrams. Medical writing support was provided by Dr. Jaya Vas, PhD, and funded by Ashirvad Institute of Pain Management and Research. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
[Table 1], [Table 2], [Table 3]
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