Trigger point injections for orofacial muscle pain: a narrative review

Introduction

It is estimated that 9.7% of the United States fits the diagnostic criteria for masticatory muscle pain (MMP) (1). It is most prevalent in females of 30–40 years in age (1,2). It has been demonstrated to cause impairment in the form of physical pain, psychological discomfort, and psychological disability (3).

MMP is usually a multifactorial condition, with different combinations of factors for each individual. Ideally, the factors are identified and eliminated, reduced, or addressed. Jaw parafunction is a significant risk factor for temporomandibular disorders (TMDs) (4), and reducing daytime parafunction through habit awareness and postural training, or addressing nocturnal parafunction with a night guard, can be effective. Stress, anxiety, depression, and distress can be causes of daytime or nocturnal parafunction, and managing those conditions or emotions through psychological therapy can be effective. Inadequate sleep can also aggravate TMD, and should therefore be addressed if present.

Often not all causative factors are identified, they cannot be reduced sufficiently to fully eliminate pain and dysfunction, or the pain has become partially centralized. Numerous treatments can still contribute to pain reduction. Stretching with self-massage, cold compresses, warm compresses (5), and cold sprays (6) are also done. Muscle relaxants and non-steroidal anti-inflammatory drugs (NSAIDs) can provide symptom relief, but should generally not be taken for more than a few months. Physical and psychological therapy (7) is also used.

When MMP is resistant to the aforementioned treatments, botulinum toxin (BTX) injections are sometimes used. The twin-block technique has also been reported as a promising option (8). Finally, trigger point injections (TPIs) can be done.

A search of the literature since 2000 revealed only one narrative review article on the topic of TPI for TMD (9). A systematic review was published in 2018, specifically comparing different injected substances and dry needling for TMD (10). As a narrative review, this manuscript aims to give the reader a broad overview of TPI for TMD by describing the pathophysiology of TPs, and the protocol, indications, contraindications, efficacy, and adverse outcomes of TPIs. We present the following article in accordance with the Narrative Review reporting checklist (available at https://joma.amegroups.com/article/view/10.21037/joma-22-5/rc).

Methods

For the section of this article on “Positive Outcomes”, source material was obtained through a PubMed literature search using the terms “trigger point injection AND (TMD OR masticatory OR jaw OR head)” (Table 1). Our inclusion criteria were studies of any type with comparison group(s) on the topic of TPIs for TMD. Studies that studied solely botulinum toxin were excluded, since the mode of action of botulinum toxin, particularly with its long duration of action on motor endplates, is significantly different from other substances injected in TPIs. No language or date limits were set.

Results

The literature search retrieved 80 potential articles (Figure 1), which were screened. Based on the abstracts, 52 articles did not meet the inclusion criteria and were excluded from the review. The full texts of 28 articles were retrieved. Reading of the full texts resulted in the exclusion of 19 more articles, and inclusion of the remaining 9. Five more articles [von Lindern et al. 2003 (11), Venâncio Rde et al. 2008 (12), Fernández-Carnero et al. 2010 (13), Dıraçoğlu et al. 2012 (14), and Silva et al. 2012 (15)] were identified through the references of the 9 included articles. Therefore, a total of 14 articles were included in this review for the section of this article on “Positive Outcomes” of TPI.

Figure 1 Flowchart of study selection process. TMD, temporomandibular disorder; TPI, trigger point injection; BTX, botulinum toxin.

Of the excluded articles, 40 were regarding TPI that was not used for TMD, 10 studied solely BTX, 7 did not involve TPIs, 8 were reviews, 1 was regarding bisphosphonates, 1 used only cadavers, and 1 was a case report. Of the included studies, 6 utilized both random allocation and blinding, 4 utilized random allocation but not blinding, 1 utilized blinding but not random allocation, 2 were retrospective and did not utilize random allocation or blinding, and 1 was prospective and did not utilize random allocation or blinding.

For the remainder of this article, the reviews, as well as their references, were used as source material.

Discussion

Trigger points (TP)

TPs were first described by Ralph Stockman in 1904 (16), though he did not name them as such. Since then, various authors have investigated and reported on TPs, with the most prolific being Janet Travell (17). Travell and Rinzler were the first to use the term “trigger points” in their 1952 publication (18).

TPs are taut bands of contracted or shortened muscle fibers (19), millimeters in diameter, which refer pain when palpated or aggravated by muscle activity (9). Typical symptoms are pain, stiffness, decreased range of motion (ROM) (20), weakness, and increased fatigability (6). Pain, usually dull or aching in quality, may occur only with aggravation, or may be continuous and worsened with aggravation. Aggravators include eating, opening, and oral parafunction. Severe pain may have a sharp quality (5).

During the physical examination, palpation of MMP patients may reveal taut and tender bands of muscle fibers 1–4 mm in diameter. Palpation along these bands may lead to the most tender point, usually no longer than several millimeters. When palpated, these TPs elicit pain and may twitch (21). The pain may be localized to the site of palpation, or may spread or refer. Spreading is the phenomenon in which pain spreads beyond the TP, but remains within the same muscle. In referral, pain is felt beyond the painful muscle (22). For example, a painful masseter muscle may refer to the molars. Referred pain is often felt in the eyes and ears. According to the Diagnostic Criteria for TMD, pressure of 1 kg for 5 seconds (22) must be applied to detect referral patterns, though some have recommended 2–4 kg/cm² for at least 6–10 seconds (23). Palpation of the TP may also decrease the pain in the referral zone (6).

The pathophysiology of TPs is still under investigation. Overload, damage, and stress may be causative factors (24). The tautness of TPs may due to a localized inflammatory mileu, which triggers the release of calcitonin gene-related peptide, inhibiting acetylcholine esterase or upregulating acetylcholinesterase receptors, and thereby increasing acetylcholine (ACh) activity. The localized acidic environment also increases ACh activity. Excessive ACh causes sustained contraction, resulting in taut bands. The tautness of the bands may inhibit blood flow locally, resulting in an energy crisis, decreasing the production of adenosine triphosphate (ATP). ATP is necessary for calcium reuptake, so a contraction is further sustained. The pain of TPs may be due to both peripheral and central sensitization. Damaged muscle tissue has been demonstrated to have inflammatory mediators and an acidic pH, both of which may sensitize peripheral nociceptors. Sustained peripheral noxious input is known to cause central sensitization (5).

The mechanism of referred pain is not entirely clear (25). According to the Convergent Projection Theory, peripheral neurons from various sites converge on common spinal neurons; the cerebral cortex thus can mistakenly assign pain to a healthy site. The Convergence-Facilitation Theory proposes that peripheral noxious input creates an irritable area in the central nervous system, which may alter the perception of non-noxious sensory input as noxious. According to the Hyperexcitability Theory, nociceptive input may open latent neural connections between sites.

The causes for TP formation are also not entirely clear. Acute trauma, or repeated microtrauma, has been proposed (26). Microtrauma, such as jaw parafunction, or occupations that require frequent use of the jaw, may be settings in which functional demands exceed the muscle’s capacity to adapt (5).

Objective of TPI

The objective of TPI is to temporarily relax the TP, allowing for improved ROM, and thereby better perfusion, nourishment, and removal of metabolic waste, breaking the pain cycle (27,28). The limitation caused by TPs is considered a perpetuator of TPs (6).

Mechanism of TPI

It is theorized that the mechanism of action of TPI is through mechanical disruption of the TP (6), then breaking the vicious cycle of spasm-pain-spasm (29). The stimulation may also affect the somatosensory thresholds (30), or reduce electrical activity, to reduce pain (31).

Indications for TPI

Numerous treatments exist for MMP, so TPI are not necessarily the first line of treatment. Ideally, as stated earlier, causative factors are identified first, and reduced or eliminated. When MMP still remains, TPI may be considered, as well as the other treatment options previously mentioned. TPI is indicated in patients who have achieved inadequate pain relief or restoration of function from other treatments. It also may be indicated for those who have not complied well with those treatments, as less commitment is needed on the patient’s part. Finally, it may be considered in patients who have severe pain in need of rapid relief.

Contraindications for TPI

Pregnancy is considered a relative contraindication; other non-pharmacological options can be considered or enhanced. If the patient is taking anticoagulants, including Aspirin, or has a history of keloid formation, the decision to inject or not inject should be made with the patient’s physician. If the TP is near a high-risk structure, the TPI may need to be reconsidered (32).

An active infection at the site of injection (32), or acute trauma to the muscle are absolute contraindications to TPI (33). TPIs should also be avoided in those with a bleeding disorder or allergy to anesthetic.

Technique of TPI

Measurement of the ROM before TPI can be helpful in gauging efficacy on an individual basis (21). A 1.25–1.5 inch needle is preferred, to ensure adequate length to reach the TP from an acute angle, though ¾ inch needles are sometimes used (34). The needle thickness should be 25 or 27 gauge (33); narrower needles may be deflected by firm the TP, rather than penetrate it (21), though they are used (34). Various contents for the syringe have been reported: anesthetic without epinephrine, sodium bicarbonate 5% buffer, dextrose 5% in water, sterile saline, triamcinolone, and dexamethasone (9).

The patient may be sitting or lying down for the injection, depending on the muscle being injected (9), but should be comfortable (33). The injection site is cleansed with alcohol or chlorhexidine. The TP is then located by palpation, ideally by a twitch, then held in a pincer fashion with one hand (9); holding the TP reduces the likelihood of it rolling aside when contacted by the needle (33). Both during localization and injection of TP in the masticatory muscles, the jaw should be propped widely open (21). The TP should then be cleansed with alcohol, betadine, or 4% chlorhexidine. The needle is then inserted at a 30 degree angle toward the TP; this usually means the skin would be penetrated approximately 1–2 cm from the TP (33) (Figures 2,3).

Figure 2 Masseter muscle. (A) Anatomy of the masseter muscle, which originates at the zygomatic arch and inserts at the mandible. (B) Injection of the masseter muscle, with the trigger point stabilized by pincer palpation, and the needle inserted at a 30-degree angle, approximately 1–2 cm from the trigger point.

Figure 3 Temporalis muscle. (A) Anatomy of the temporalis muscle, which originates at the temporal fossa, and inserts on the coronoid process of the mandible, as well as the anterior border of the mandibular ramus. (B) Injection of the temporalis muscle, with the trigger point stabilized by pincer palpation, and the needle inserted at a 30-degree angle, approximately 1–2 cm from the trigger point.

The needle is inserted and retracted repeatedly, without fully removing tip from skin, from multiple directions in a fan shape (21,33), slowly delivering the contents throughout, until the twitching has subsided, or muscle adequately relaxed. Crunching or pulling may be felt in the beginning of the process (9). Approximately 1–2 mL of solution is typically used at each TP (33). Once the injection is complete, the patient should gently move the affected structure in its full ROM in all directions (21,33), to initiate perfusion of the muscle. It is advised that this movement is done three times during the appointment.

Following the injection, the patient may apply ice to the TPI areas for a few hours, and should be told that soreness may persist for 3–4 days. The structure should continue to be routinely move the jaw gently and fully in the days following the appointment, to maintain the ROM gained and to allow fuller perfusion of the muscle, the muscle should not be over-used for 3–4 days (33).

Some details when injecting masticatory muscles warrant mention (Figures 2,3). The medial pterygoid muscle rarely requires TPI, since it responds well to spray and stretch. When the medial pterygoid or lateral pterygoid muscles are injected, the approach can be extraoral or intraoral. Extraoral access is from below the zygomatic arch and between the mandibular condyle and coronoid process (21). Intraoral access is through the pharyngeal wall for the medial pterygoid muscle. For the lateral pterygoid muscle, intraoral access starts distal to the second maxillary molar, and proceeds in a distopalatal direction (35). When injecting the temporalis muscle, the temporal artery should be first identified and avoided (21).

Positive outcomes

In a randomized, double-blind study, Sabatke et al. compared a single TPI with 2% lidocaine LA (n=21), and single TPI with 0.9% saline (n=26), and no TPI (n=23), evaluating their effects 15 days post-injection. Both local anesthetic (LA) and saline TPI statistically significantly decreased facial pain, headache pain, and headache frequency, but there was no significant difference between groups. The control group had no significant improvement in any of the parameters (36).

A systematic review by Machado et al. (10) assessed the effect of different TPI techniques, and TPI versus other treatments. In a randomized, double-blind, double-placebo study, McMillan et al. compared 1% procaine and simulated dry-needling (n=10), dry needling and simulated LA using saline (n=10), and simulated LA and simulated dry needling (n=10). Injections were performed in the masseter muscle, once a week for 3 weeks, and assessment was performed before and after each session. None of the groups experienced an increase in PPT. All groups had statistically significant decreases in pain intensity and pain unpleasantness, but there were no significant differences between groups (30).

When dry needling (once per week for 3 weeks) in 24 subjects was compared to a combination of 760 mg methocarbamol and 600 mg paracetamol (every 6 hours for 3 weeks) in 24 subjects, in a randomized blinded clinical trial, both groups demonstrated statistically significant reductions in pain at rest and with mastication, when assessed 2 and 8 weeks after completion of treatment. The dry needling group also performed statistically significantly better than the methocarbamol and paracetamol group for improving pain at rest and with mastication, latertrusive range, and protrusive range (11).

Whether TPI was performed with injection of a substance, or without injection of a substance (“dry needling”), pain intensity, frequency, and duration decreased. However, there were no statistically significant differences between TPI with and without injected substances (12,15).

When Fernández-Carnero et al. compared dry needling to false needling (using a short needle) in a randomized double-blind cross-over study of 12 subjects, dry needling demonstrated a statistically significant improvement in the PPT and maximum mouth opening (MMO) at the 5 minute post-injection assessment (13). When Dıraçoğlu et al. compared dry needling in 25 subjects to false needling (needling a region without a TP) in 25 subjects in a randomized double-blind parallel trial, with needling being performed 3 times at 7-day intervals, dry needling demonstrated a statistically significant improvement in palpation pain threshold (PPT), but not MMO or pain measured on the visual analog scale (VAS), at the 1-week assessment (14).

Non-randomized and non-blinded studies have also been done, though their findings should be interpreted with consideration for their weaker study design. Ozkan et al. compared SS (worn for 3 months) in 25 subjects to SS and TPI (first two injection sessions with 0.5 mL lidocaine and 0.5 mL saline; third injection session with 0.1 mL triamcinolone acetonide) in 25 subjects in a randomized non-blinded trial at 2, 4, and 12 weeks after treatment was completed. Both groups saw statistically significant reductions in the frequency and intensity of pain, number of TP, number of patients with myofascial orofacial pain at rest, and number of patients with myofascial orofacial pain with movement. The group that received stabilization splints (SS) and TPI also had statistically significantly less pain with movement than the SS group (37).

Gupta et al. compared TPI (given once, using 0.5% bupivacaine) in 37 subjects to TPI and levosulpiride (50 mg twice a day for 2 weeks, then increased to a maximum of thrice daily for a maximum of 6 weeks) in 36 subjects, in a randomized non-blinded trial. Assessment was performed at weeks 1, 4, 6, and 12. VAS and depression significantly decreased for both groups at all points. The group that received TPI and levosulpiride had significantly more VAS reduction than the group that received only TPI, at the 4-, 6-, and 12-week points, and significantly more depression reduction at the 6- and 12-week points (38).

Bilici et al., in a non-blinded, non-randomized retrospective cohort study, compared SS (29 subjects) to SS + TPI 3 times, on alternate days (12 subjects), and to SS + TPI 3 times, once a week (15 subjects). The group that received injections on alternate days performed significantly better than the other groups for VAS reduction (29).

Okada-Ogawa A, in a single-blinded study compared TPI done three times, one week apart (10 subjects) to massage and stretch at home for 2 weeks (10 subjects). TPI with massage & stretch significantly decreased VAS, but only massage & stretch significantly decreased taut band hardness. Patients may feel immediate pain reduction, which may wane by 2 weeks later (39).

A non-blinded retrospective cohort study by Yilmaz et al. compared TPI with mepivacaine 3% LA (n=21), BTX (n=26), and platelet-rich plasma (PRP) (n=29). Injections were performed once, and assessed 1 month, 3, and 6 months post-injection. At 1 month and 3 months, all groups had statistically significant improvements in pain, jaw function limitation, and self-reported discomfort, and disability due to oral conditions. Groups receiving LA and BTX performed better in those parameters than the group receiving PRP at 3 months. The BTX group performed better in those parameters than the LA group at 3 months. By 6 months, only the BTX group still had significant improvement in any of those parameters (40).

Sakalys et al., in a randomized, non-blinded prospective study, compared TPI in the masseter muscle using 2% lidocaine (n=25) and PRP (n=25). Both groups had statistically significant improvement in VAS at 4 weeks post-injection, but not at 2 weeks post-injection. The PRP injection also performed statistically significantly better than the LA injection for VAS reduction at 4 weeks post-injection, but not at 2 weeks post-injection (41).

Taşkesen et al. compared the masseteric nerve block (n=15), TPI with 2% lidocaine (n=15), and dry needling with acupuncture needles (n=15) in a non-blinded study. The random allocation methodology was not clear enough to determine its adequacy. At 12 weeks, all groups had significant increases in maximum opening, but the dry needling and TPI with lidocaine groups had significantly more improvement in pain on function compared to masseteric nerve block group. However, while the dry needling and lidocaine TPI were performed twice with a 7-day interval, it is unclear how many times the masseteric nerve block was administered (34).

The positive outcomes are summarized in Table 2.

Negative outcomes

Hammi et al. listed adverse effects that can occur with TPIs, which include pain, bleeding, infection, allergy or systemic toxicity to the anesthetic, hematoma, vascular injury, and a vasovagal and syncopal response (9). Severe cramping in the general region of the injection may occur, and is usually due to shortening activation of the antagonist muscle; it can be avoided by also injecting the antagonist muscle. Pain occurs during the injection initially; hyperalgesic patients may have less pain with a smaller gauge needle, though if it is too narrow, it may deflect off the TP, rather than penetrate it (21).

However, it should be noted that none of the studies included in this review reported negative outcomes. Machado et al., in a systematic review, likewise noted no adverse effects in any of the included studies, except those studied Botox injections (10).

Conclusions

There is evidence that TPI may improve MMP symptoms and jaw function, though the evidence is not strong. The evidence also does not conclusively indicate any injected substance, or any substance at all, to be superior. Larger randomized, blinded, controlled studies are needed to determine whether TPIs are effective, and if so, the specific methods and substances that are effective.

Acknowledgments

The authors would like to thank Shilpa Padar Shastry and Shruthi Anil for creating Figures 2,3.

Funding: None.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editor (Mythili Kalladka) for the series “Orofacial Pain: Diagnostic and Therapeutic Topicals, Nerve Blocks and Trigger Point Injection” published in Journal of Oral and Maxillofacial Anesthesia. The article has undergone external peer review.

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://joma.amegroups.com/article/view/10.21037/joma-22-5/rc

Peer Review File: Available at https://joma.amegroups.com/article/view/10.21037/joma-22-5/prf

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://joma.amegroups.com/article/view/10.21037/joma-22-5/coif). The series “Orofacial Pain: Diagnostic and Therapeutic Topicals, Nerve Blocks and Trigger Point Injection” was commissioned by the editorial office without any funding or sponsorship. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Manfredini D, Guarda-Nardini L, Winocur E, et al. Research diagnostic criteria for temporomandibular disorders: a systematic review of axis I epidemiologic findings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112:453-62. [Crossref] [PubMed]
2. Leeuw R de, Klasser GD. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management (AAOP The American Academy of Orofacial Pain), 6th Edition. 6th edition. Hanover Park, IL: CBS, 2018:336.
3. Hanna K, Nair R, Amarasena N, et al. Temporomandibular dysfunction experience is associated with oral health-related quality of life: an Australian national study. BMC Oral Health 2021;21:432. [Crossref] [PubMed]
4. Slade GD, Ohrbach R, Greenspan JD, et al. Painful Temporomandibular Disorder: Decade of Discovery from OPPERA Studies. J Dent Res 2016;95:1084-92. [Crossref] [PubMed]
5. Kalladka M, Young A, Khan J. Myofascial pain in temporomandibular disorders: Updates on etiopathogenesis and management. J Bodyw Mov Ther 2021;28:104-13. [Crossref] [PubMed]
6. Fricton JR. Management of masticatory myofascial pain. Semin Orthod 1995;1:229-43. [Crossref] [PubMed]
7. List T, Axelsson S. Management of TMD: evidence from systematic reviews and meta-analyses. J Oral Rehabil 2010;37:430-51. [Crossref] [PubMed]
8. Quek SYP, Gomes-Zagury J, Subramanian G. Twin Block in Myogenous Orofacial Pain: Applied Anatomy, Technique Update, and Safety. Anesth Prog 2020;67:103-6. [Crossref] [PubMed]
9. Hammi C, Schroeder JD, Yeung B. Trigger Point Injection. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 [cited 2022 Jan 15]. Available online: http://www.ncbi.nlm.nih.gov/books/NBK542196/
10. Machado E, Machado P, Wandscher VF, et al. A systematic review of different substance injection and dry needling for treatment of temporomandibular myofascial pain. Int J Oral Maxillofac Surg 2018;47:1420-32. [Crossref] [PubMed]
11. von Lindern JJ, Niederhagen B, Bergé S, et al. Type A botulinum toxin in the treatment of chronic facial pain associated with masticatory hyperactivity. J Oral Maxillofac Surg 2003;61:774-8. [Crossref] [PubMed]
12. Venâncio Rde A, Alencar FG, Zamperini C. Different substances and dry-needling injections in patients with myofascial pain and headaches. Cranio 2008;26:96-103. [Crossref] [PubMed]
13. Fernández-Carnero J, La Touche R, Ortega-Santiago R, et al. Short-term effects of dry needling of active myofascial trigger points in the masseter muscle in patients with temporomandibular disorders. J Orofac Pain 2010;24:106-12. [PubMed]
14. Dıraçoğlu D, Vural M, Karan A, et al. Effectiveness of dry needling for the treatment of temporomandibular myofascial pain: a double-blind, randomized, placebo controlled study. J Back Musculoskelet Rehabil 2012;25:285-90. [Crossref] [PubMed]
15. Silva ROF, Conti PCR, Araújo CDRP, et al. Evaluation of dry needling and 0.5% lidocaine injection therapies in myofascial pain trigger points in masticatory muscles. Dental Press J Orthod 2012;17:113-8. [Crossref]
16. Stockman R. The Causes and Treatment of Chronic Rheumatism. Br Med J 1904;1:477-9. [Crossref] [PubMed]
17. Shah JP, Thaker N, Heimur J, et al. Myofascial Trigger Points Then and Now: A Historical and Scientific Perspective. PM R 2015;7:746-61. [Crossref] [PubMed]
18. Travell J, Rinzler SH. The myofascial genesis of pain. Postgrad Med 1952;11:425-34. [Crossref] [PubMed]
19. Chen Q, Basford J, An KN. Ability of magnetic resonance elastography to assess taut bands. Clin Biomech (Bristol, Avon) 2008;23:623-9. [Crossref] [PubMed]
20. Lavelle ED, Lavelle W, Smith HS. Myofascial trigger points. Med Clin North Am 2007;91:229-39. [Crossref] [PubMed]
21. Travell JG, Simons DG. Myofascial Pain And Dysfunction - The Trigger Point Manual. Williams & Wilkins, 1983.
22. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) for Clinical and Research Applications: recommendations of the International RDC/TMD Consortium Network* and Orofacial Pain Special Interest Group†. J Oral Facial Pain Headache 2014;28:6-27. [Crossref] [PubMed]
23. Jaeger B. Myofascial trigger point pain. Alpha Omegan 2013;106:14-22. [PubMed]
24. Gupta P, Singh V, Sethi S, et al. A Comparative Pilot Study to Evaluate the Adjunctive Role of Levosulpride with Trigger Point Injection Therapy in the Management of Myofascial Pain Syndrome of Orofacial Region. J Maxillofac Oral Surg 2014;13:599-602. [Crossref] [PubMed]
25. Arendt-Nielsen L, Svensson P. Referred muscle pain: basic and clinical findings. Clin J Pain 2001;17:11-9. [Crossref] [PubMed]
26. Alvarez DJ, Rockwell PG. Trigger points: diagnosis and management. Am Fam Physician 2002;65:653-60. [PubMed]
27. Wong CS, Wong SH. A new look at trigger point injections. Anesthesiol Res Pract 2012;2012:492452. [Crossref] [PubMed]
28. Ricci V, Özçakar L. Ultrasound imaging of the upper trapezius muscle for safer myofascial trigger point injections: a case report. Phys Sportsmed 2019;47:247-8. [Crossref] [PubMed]
29. Bilici IŞ, Emes Y, Aybar B, et al. Evaluation of the effects of occlusal splint, trigger point injection and arthrocentesis in the treatment of internal derangement patients with myofascial pain disorders. J Craniomaxillofac Surg 2018;46:916-22. [Crossref] [PubMed]
30. McMillan AS, Nolan A, Kelly PJ. The efficacy of dry needling and procaine in the treatment of myofascial pain in the jaw muscles. J Orofac Pain 1997;11:307-14. [PubMed]
31. Chen JT, Chung KC, Hou CR, et al. Inhibitory effect of dry needling on the spontaneous electrical activity recorded from myofascial trigger spots of rabbit skeletal muscle. Am J Phys Med Rehabil 2001;80:729-35. [Crossref] [PubMed]
32. Robbins MS, Kuruvilla D, Blumenfeld A, et al. Trigger point injections for headache disorders: expert consensus methodology and narrative review. Headache 2014;54:1441-59. [Crossref] [PubMed]
33. Trigger Point Injection [Internet]. [cited 2022 Jan 10]. Available online: https://fpnotebook.com/rheum/procedure/TrgrPntInjctn.htm
34. Taşkesen F, Cezairli B. The effectiveness of the masseteric nerve block compared with trigger point injections and dry needling in myofascial pain. Cranio 2020; Epub ahead of print. [Crossref] [PubMed]
35. Mor N, Tang C, Blitzer A. Temporomandibular Myofacial Pain Treated with Botulinum Toxin Injection. Toxins (Basel) 2015;7:2791-800. [Crossref] [PubMed]
36. Sabatke S, Scola RH, Paiva ES, et al. Injecction of trigger points in the temporal muscles of patients with miofascial syndrome. Arq Neuropsiquiatr 2015;73:861-6. [Crossref] [PubMed]
37. Ozkan F, Cakır Özkan N, Erkorkmaz U. Trigger point injection therapy in the management of myofascial temporomandibular pain. Agri 2011;23:119-25. [Crossref] [PubMed]
38. Gupta P, Singh V, Sethi S, et al. A Comparative Study of Trigger Point Therapy with Local Anaesthetic (0.5% Bupivacaine) Versus Combined Trigger Point Injection Therapy and Levosulpiride in the Management of Myofascial Pain Syndrome in the Orofacial Region. J Maxillofac Oral Surg 2016;15:376-83. [Crossref] [PubMed]
39. Okada-Ogawa A, Sekine N, Watanabe K, et al. Change in muscle hardness after trigger point injection and physiotherapy for myofascial pain syndrome. J Oral Sci 2019;61:36-44. [Crossref] [PubMed]
40. Yilmaz O, Sivrikaya EC, Taskesen F, et al. Comparison of the Efficacy of Botulinum Toxin, Local Anesthesia, and Platelet-Rich Plasma Injections in Patients With Myofascial Trigger Points in the Masseter Muscle. J Oral Maxillofac Surg 2021;79:88.e1-9. [Crossref] [PubMed]
41. Sakalys D, Rokicki JP, Januzis G, et al. Plasma rich in growth factors injection effectiveness for myofascial pain treatment in masticatory muscles. Randomised controlled trial. J Oral Rehabil 2020;47:796-801. [Crossref] [PubMed]