Overview of Myofascial Injections
Myofascial pain is a common source of pain in the neck, low back region, and other areas of the body. The term “myofascial pain” encompasses muscle strain, myofascial trigger points, and specific muscle pain syndromes, including piriformis syndrome, iliopsoas-related pain, and pain related to compression of the brachial plexus by the scalene muscles (neurogenic thoracic outlet syndrome).
Relevant Anatomy
Skeletal muscle consists of muscle fibers under somatic nervous control. Each nerve root innervates a muscle or group of muscles known as a myotome. The muscle belly of skeletal muscles is connected by tendons to the bone. Trigger points occur in the body of the muscle, most often located in the center of the muscle.
Trigger Point Injections
Trigger points are nodules found in taut bands in skeletal muscle that often produce characteristic patterns of referred pain provoked by palpation. A trigger point may occur in isolation, concomitantly as part of a regional myofascial pain syndrome, or as an effect of other pain syndromes through either segmental effects or biomechanical changes. Trigger points are diagnosed by the history and physical examination. A patient will complain of a localized pain or regional pain in or around skeletal muscle or replicated by palpation of a skeletal muscle. The muscles commonly involved are the trapezius, splenii, cervical and lumbar paraspinal, and quadratus lumborum. On examination, localized taut bands of muscle are noted and palpation produces characteristic nondermatomal referral patterns. Trigger points may be active or latent. Active trigger points produce spontaneous pain and are painful on palpation, whereas latent trigger points produce pain only when palpated. Trigger points may result from trauma, overload or overuse injury, or a prolonged period during which the muscle is in a shortened position. The pathophysiology of trigger points is not fully understood, although multiple lines of relevant research support their existence. Peripheral sensitization and central sensitization both appear to contribute to the pain from trigger points. There is also evidence of an alteration in blood flow at trigger points.
Imaging studies have only recently demonstrated anatomic changes associated with trigger points. Ultrasound (US) examination in combination with Doppler blood flow has been reported to allow visualization of trigger points, and US imaging can help direct muscle injection techniques (see later). Recently developed techniques using magnetic resonance and US elastography purport to reveal changes in intramuscular signal consistent with trigger points, but this technology has not yet been validated.
Treatment of trigger points commonly includes physical therapy (manual release techniques, stretching and strengthening, conditioning, therapeutic modalities), trigger point injections (TPIs), dry needling and acupuncture, and transcutaneous electrical nerve stimulation. A broad range of treatment modalities have been reported, but weak research methodology continues to limit interpretation of the results. Regarding medications, tizanidine, but not cyclobenzaprine, was noted to be efficacious for acute skeletal muscle spasms. Diazepam, amitriptyline, and lidocaine patch were found to be effective, but literature support for the use of anticonvulsants in treating myofascial pain syndrome is limited. Although clonazepam appears to be effective, its use is limited by the side effects of depression, liver dysfunction, and difficulty weaning the patient from this drug. Nonsteroidal anti-inflammatory drugs (NSAIDs), specifically ibuprofen, appear to be effective when given with other agents, but not as monotherapy.
TPIs are intramuscular injections of local anesthetic with or without corticosteroid. Some practitioners perform dry needling (needle penetration without infiltration of medication), and there is evidence that dry needling can be as effective as TPI but may cause more muscle soreness. The response to TPI or dry needling is more effective when a muscle twitch reaction is elicited with needle penetration of the trigger point. Some authors have suggested that botulinum toxin or tropisetron (a serotonin 5-HT 3 receptor antagonist) can be used for TPI, but the superiority of alternatives over more conventional injectants has not been consistently demonstrated.
Contraindications
The following conditions are contraindications to TPI: (1) infection, systemic or localized; (2) coagulopathy; (3) distorted or complicated anatomy; and (4) patient refusal.
Technique and Follow-Up
After informed consent, the muscle is palpated and the trigger points are identified and marked. The area is prepared in sterile fashion and a 25-gauge, 1.5-inch needle is inserted into the trigger point. A local twitch may be elicited at this time or the patient verbally identifies the painful area. After negative aspiration, 0.25% bupivacaine, 0.2% ropivacaine, or 1% lidocaine is injected with or without steroid, either dexamethasone (4 mg in a 30-mL bottle of local anesthetic) or a low dose of particulate steroid (e.g., 20 to 40 mg of methylprednisolone or triamcinolone diluted in the local anesthetic solution).
Possible complications include bleeding, hematoma, nerve block, and infection. The patient should be monitored closely for bleeding, development of neurologic symptoms (numbness or weakness, urinary or bowel incontinence), or signs of infection. Depending on the location of the injection, the patient should be instructed on the signs and symptoms of pneumothorax (from neck, shoulder, thoracic, and anterior chest wall injections) or local nerve blockade (for example, inadvertent median nerve block with injection of the flexor carpi ulnaris).
The success of the procedure is dependent on the diagnosis and localization of the trigger point. Patients with chronic widespread pain or psychological disorders are less likely to respond to TPI only. Patients who have focal muscle pain with the characteristics of myofascial pain can achieve significant relief for days to months with a well-performed TPI. Success of TPI is often dependent on subsequent stretching and strengthening and neuromuscular education of the muscle. The most effective treatment of myofascial pain syndrome is often a multidisciplinary approach tailored to the individual needs of the patient that incorporates TPI with physical therapy and medication as noted earlier. Practitioners are counseled to provide appropriate follow-up after TPI and encourage patients to address other factors that perpetuate chronic pain (coping, employment, decreased social activity).
Ultrasound-Guided Techniques
US guidance provides several theoretical advantages over blind needle insertion. As stated, it allows visualization of the trigger point ( Fig. 64.1 ). The practitioner is ensured that the needle is penetrating muscle tissue, which may be of use in patients with considerable adipose tissue, and can avoid local anatomic structures that are sensitive to needle penetration or local anesthetic infiltration (i.e., neurovascular structures or viscera). US imaging also allows visualization of the muscle twitch response with needle penetration, especially in muscles that are deep or small. An additional use of US is to confirm local anesthetic infiltration between fascial planes. It also aids in blocking the spinal accessory nerve for diagnosis of trapezius muscle–related myofascial pain.
Results of Treatment
Research on treatment outcomes of myofascial pain has been limited by poor study methodology and reporting, inconsistent outcome selection, small sample sizes, heterogeneous patient populations, and the absence of standardized diagnostic criteria (with the exception of validated diagnostic criteria for myofascial pain of the muscles of the jaw). Overall, evidence from systematic reviews supports the finding that TPI (regardless of the injectant) and dry needling of trigger points provide a benefit alone and in addition to stretching and strengthening. Deep dry needling appears to be more effective than superficial dry needling.
Several well-designed studies have evaluated the use of botulinum toxin for the treatment of myofascial pain, but with conflicting conclusions: although some found positive results, the preponderance did not find statistically significant effects of botulinum toxin over saline or local anesthetic. In fact, a qualitative review of published trials on botulinum toxin for myofascial TPI noted its lack of efficacy. Tropisetron, a 5-HT 3 receptor antagonist, may offer longer analgesic effect than occurs with local anesthetic.
Combining medication management with physical therapy and injection therapy can often offer the best opportunity for treatment. Treatment with amitriptyline, benzodiazepines, and ibuprofen (in combination with other agents) appears to be effective, and preliminary data support topical rubefacient patches, diclofenac patches, and lidocaine patches. Duloxetine has recently been given an indication for musculoskeletal pain; it will probably be commonly used for the treatment of myofascial pain. The prescription of benzodiazepines must be brief and goal directed, with due diligence to minimize misuse, addiction, and diversion.
Factors associated with a lower therapeutic effect of TPI include poor coping, employment issues, decreased social activity, duration of the pain syndrome, high levels of pain, constant pain (as opposed to intermittent pain), and unresponsiveness of the pain to analgesic medication.
Trigger Point Injections
Trigger points are nodules found in taut bands in skeletal muscle that often produce characteristic patterns of referred pain provoked by palpation. A trigger point may occur in isolation, concomitantly as part of a regional myofascial pain syndrome, or as an effect of other pain syndromes through either segmental effects or biomechanical changes. Trigger points are diagnosed by the history and physical examination. A patient will complain of a localized pain or regional pain in or around skeletal muscle or replicated by palpation of a skeletal muscle. The muscles commonly involved are the trapezius, splenii, cervical and lumbar paraspinal, and quadratus lumborum. On examination, localized taut bands of muscle are noted and palpation produces characteristic nondermatomal referral patterns. Trigger points may be active or latent. Active trigger points produce spontaneous pain and are painful on palpation, whereas latent trigger points produce pain only when palpated. Trigger points may result from trauma, overload or overuse injury, or a prolonged period during which the muscle is in a shortened position. The pathophysiology of trigger points is not fully understood, although multiple lines of relevant research support their existence. Peripheral sensitization and central sensitization both appear to contribute to the pain from trigger points. There is also evidence of an alteration in blood flow at trigger points.
Imaging studies have only recently demonstrated anatomic changes associated with trigger points. Ultrasound (US) examination in combination with Doppler blood flow has been reported to allow visualization of trigger points, and US imaging can help direct muscle injection techniques (see later). Recently developed techniques using magnetic resonance and US elastography purport to reveal changes in intramuscular signal consistent with trigger points, but this technology has not yet been validated.
Treatment of trigger points commonly includes physical therapy (manual release techniques, stretching and strengthening, conditioning, therapeutic modalities), trigger point injections (TPIs), dry needling and acupuncture, and transcutaneous electrical nerve stimulation. A broad range of treatment modalities have been reported, but weak research methodology continues to limit interpretation of the results. Regarding medications, tizanidine, but not cyclobenzaprine, was noted to be efficacious for acute skeletal muscle spasms. Diazepam, amitriptyline, and lidocaine patch were found to be effective, but literature support for the use of anticonvulsants in treating myofascial pain syndrome is limited. Although clonazepam appears to be effective, its use is limited by the side effects of depression, liver dysfunction, and difficulty weaning the patient from this drug. Nonsteroidal anti-inflammatory drugs (NSAIDs), specifically ibuprofen, appear to be effective when given with other agents, but not as monotherapy.
TPIs are intramuscular injections of local anesthetic with or without corticosteroid. Some practitioners perform dry needling (needle penetration without infiltration of medication), and there is evidence that dry needling can be as effective as TPI but may cause more muscle soreness. The response to TPI or dry needling is more effective when a muscle twitch reaction is elicited with needle penetration of the trigger point. Some authors have suggested that botulinum toxin or tropisetron (a serotonin 5-HT 3 receptor antagonist) can be used for TPI, but the superiority of alternatives over more conventional injectants has not been consistently demonstrated.
Contraindications
The following conditions are contraindications to TPI: (1) infection, systemic or localized; (2) coagulopathy; (3) distorted or complicated anatomy; and (4) patient refusal.
Technique and Follow-Up
After informed consent, the muscle is palpated and the trigger points are identified and marked. The area is prepared in sterile fashion and a 25-gauge, 1.5-inch needle is inserted into the trigger point. A local twitch may be elicited at this time or the patient verbally identifies the painful area. After negative aspiration, 0.25% bupivacaine, 0.2% ropivacaine, or 1% lidocaine is injected with or without steroid, either dexamethasone (4 mg in a 30-mL bottle of local anesthetic) or a low dose of particulate steroid (e.g., 20 to 40 mg of methylprednisolone or triamcinolone diluted in the local anesthetic solution).
Possible complications include bleeding, hematoma, nerve block, and infection. The patient should be monitored closely for bleeding, development of neurologic symptoms (numbness or weakness, urinary or bowel incontinence), or signs of infection. Depending on the location of the injection, the patient should be instructed on the signs and symptoms of pneumothorax (from neck, shoulder, thoracic, and anterior chest wall injections) or local nerve blockade (for example, inadvertent median nerve block with injection of the flexor carpi ulnaris).
The success of the procedure is dependent on the diagnosis and localization of the trigger point. Patients with chronic widespread pain or psychological disorders are less likely to respond to TPI only. Patients who have focal muscle pain with the characteristics of myofascial pain can achieve significant relief for days to months with a well-performed TPI. Success of TPI is often dependent on subsequent stretching and strengthening and neuromuscular education of the muscle. The most effective treatment of myofascial pain syndrome is often a multidisciplinary approach tailored to the individual needs of the patient that incorporates TPI with physical therapy and medication as noted earlier. Practitioners are counseled to provide appropriate follow-up after TPI and encourage patients to address other factors that perpetuate chronic pain (coping, employment, decreased social activity).
Ultrasound-Guided Techniques
US guidance provides several theoretical advantages over blind needle insertion. As stated, it allows visualization of the trigger point ( Fig. 64.1 ). The practitioner is ensured that the needle is penetrating muscle tissue, which may be of use in patients with considerable adipose tissue, and can avoid local anatomic structures that are sensitive to needle penetration or local anesthetic infiltration (i.e., neurovascular structures or viscera). US imaging also allows visualization of the muscle twitch response with needle penetration, especially in muscles that are deep or small. An additional use of US is to confirm local anesthetic infiltration between fascial planes. It also aids in blocking the spinal accessory nerve for diagnosis of trapezius muscle–related myofascial pain.
Results of Treatment
Research on treatment outcomes of myofascial pain has been limited by poor study methodology and reporting, inconsistent outcome selection, small sample sizes, heterogeneous patient populations, and the absence of standardized diagnostic criteria (with the exception of validated diagnostic criteria for myofascial pain of the muscles of the jaw). Overall, evidence from systematic reviews supports the finding that TPI (regardless of the injectant) and dry needling of trigger points provide a benefit alone and in addition to stretching and strengthening. Deep dry needling appears to be more effective than superficial dry needling.
Several well-designed studies have evaluated the use of botulinum toxin for the treatment of myofascial pain, but with conflicting conclusions: although some found positive results, the preponderance did not find statistically significant effects of botulinum toxin over saline or local anesthetic. In fact, a qualitative review of published trials on botulinum toxin for myofascial TPI noted its lack of efficacy. Tropisetron, a 5-HT 3 receptor antagonist, may offer longer analgesic effect than occurs with local anesthetic.
Combining medication management with physical therapy and injection therapy can often offer the best opportunity for treatment. Treatment with amitriptyline, benzodiazepines, and ibuprofen (in combination with other agents) appears to be effective, and preliminary data support topical rubefacient patches, diclofenac patches, and lidocaine patches. Duloxetine has recently been given an indication for musculoskeletal pain; it will probably be commonly used for the treatment of myofascial pain. The prescription of benzodiazepines must be brief and goal directed, with due diligence to minimize misuse, addiction, and diversion.
Factors associated with a lower therapeutic effect of TPI include poor coping, employment issues, decreased social activity, duration of the pain syndrome, high levels of pain, constant pain (as opposed to intermittent pain), and unresponsiveness of the pain to analgesic medication.
Piriformis Injections
Piriformis syndrome consists of pain in the buttock with or without radiation in the distribution of the ipsilateral sciatic nerve. It may contribute up to 8% of buttock pain. The syndrome can be a consequence of an abnormal relationship between the sciatic nerve and the piriformis muscle that results in irritation of the sciatic nerve. A hypertrophic muscle, infection, or invasion of the muscle by tumor can cause pressure or irritation on the nerve. In 78% to 84% of the population, the sciatic nerve passes in front of the muscle. In 12% to 21% of individuals, the divided nerve passes through or posterior to the piriformis and is exposed to muscle contractions, which trigger sciatic symptoms. Piriformis syndrome is a diagnosis of exclusion since there are no standardized diagnostic criteria for it. The syndrome should be considered in patients who have buttock pain, tenderness to palpation over the piriformis muscle, and a positive response to provocative maneuvers, including the following:
- 1.
Pace’s sign: pain and weakness with seated abduction of the hip against resistance
- 2.
Lasègue’s sign (also known as the straight-leg raise test): pain with unresisted flexion, adduction, and internal rotation of the flexed hip
- 3.
Freiberg’s sign: pain with forced (i.e., against resistance) internal rotation of the extended hip
Because of its small size in comparison to the gluteus muscles, its proximity to neurovascular structures, and its deep location, the piriformis muscle is usually injected under radiographic or US guidance. Piriformis injections under computed tomography (CT) or electromyographic guidance have also been described. Contraindications are the same as those noted in the section on TPI.
Fluoroscopic Technique
The patient is placed prone on a fluoroscopy table, and the inferior margin of the sacroiliac joint is imaged and marked. The needle insertion site is 1 to 2 cm caudal and 1 to 2 cm lateral to the inferior margin of the sacroiliac joint. After sterile preparation and infiltration of local anesthetic, a 7- to 10-cm insulated needle is inserted and advanced with the nerve stimulator turned on (1 mA, 2 Hz, 0.1 msec) until an evoked motor response of the sciatic nerve is achieved (dorsiflexion, plantar flexion, eversion, inversion) at 0.4 to 0.6 mA. The needle is then withdrawn slightly until the sciatic stimulation disappears; this is to avoid intraneural injection. Steroid (40 mg of either methylprednisolone or triamcinolone) plus 5 mL of saline is injected around the sciatic nerve—this is helpful, especially in patients with signs of sciatic nerve irritation. The needle is then pulled back 1 cm into the belly of the piriformis muscle, and 1 to 2 mL of contrast agent is injected. The contrast agent should outline the piriformis muscle belly with no sign of spillage ( Fig. 64.2 ). After the characteristic spread of dye is achieved—outline of the piriformis muscle with clean margins—the local anesthetic solution with steroid is administered. Typically, good pain relief can be attained with an injection of 5 mL of 0.25% or 0.5% bupivacaine plus 40 mg of methylprednisolone (or triamcinolone). For botulinum toxin injection, 100 mouse units in a 2-mL volume is injected.
Ultrasound-Guided Technique
The US-guided technique not only permits a direct view of the piriformis muscle but can also be used to examine its relationship to the sciatic nerve and rule out any anatomic variation. The patient is placed in the prone position with the US machine on the side opposite the operator. A curved, low-frequency US probe (2 to 6 MHz) is used to scan a wider and deeper area. The US machine should have Doppler to help identify the inferior gluteal artery medial to the sciatic nerve and anterior to the piriformis. A 20- to 22-gauge, 10- to 12-cm-long needle is recommended.
One technique involves positioning the transducer in short axis (transverse) over the sacroiliac joint, where medially the sacrum will be visible and laterally the ilium/gluteus maximus muscle complex will be observed. While keeping the sacroiliac joint in the center of the screen, the transducer is moved caudally until the lateral view of the ilium is lost, which indicates that the transducer is over the greater sciatic notch. In this position the operator will see the hyperechoic lateral portion of the sacrum medially. In the center of the image the following are visualized: skin and fat in the near field and then the gluteus maximus muscle. Deeper to the gluteus maximus and originating from the anterior and lateral sacral edge is the piriformis muscle with its typical longitudinal fibers ( Fig. 64.3 ). By moving the transducer slightly lower and mildly rotating the left gluteal area clockwise (counterclockwise on the right side), the sciatic nerve becomes visible deeper in the medial aspect of the piriformis. The ischium initially appears as a curved hyperechoic line (posterior acetabulum); more caudally it becomes a flat line deeper to the piriformis. Another way to find the piriformis is to place the transducer over the line between the greater trochanter and ischial tuberosity. Once the sciatic nerve is identified, it is followed cephalad until the piriformis and gluteus maximus muscles are seen over the sciatic nerve.
To confirm the view of the piriformis muscle, flex the patient’s knee 90 degrees and rotate the hip internally and externally. During this maneuver the piriformis will slide over the ischium while the position of the gluteus maximus remains stable. While observing the sciatic notch it is useful to identify the ischial spine since other muscles that are in similar position as the piriformis insert in the area (i.e., the gemelli and obturator muscles) and should be differentiated from it.
The piriformis runs almost horizontal between the sacrum and the femur. A lateral-to-medial, in-plane approach is ideal to maximize visualization of the needle; the needle enters the skin 3 to 4 cm lateral to the lateral edge of the transducer. The needle should cross the skin and fat in a lateral-to-medial, posterior-to-anterior direction and enter the gluteus maximus and then the piriformis in its medial half. Hydrodissection with normal saline (or a nonelectrolyte solution such as 5% dextrose if stimulation is planned) may help confirm the position of the tip of the needle. The steroid (methylprednisolone or triamcinolone) plus local anesthetic (bupivacaine or lidocaine) is then injected. After injecting the piriformis muscle, to decrease sciatic nerve irritation, the needle can be advanced and positioned between the piriformis and the sciatic nerve to create a layer of local anesthetic with steroid. Five to 8 mL of the mixture is usually adequate.
Postprocedure Follow-Up
The patient should be monitored closely for the following: (1) bleeding and bruising, (2) local infection, and (3) neurologic symptoms (leg numbness and weakness, urinary or bowel incontinence). It is not uncommon for weakness or numbness to develop in the distribution of the sciatic nerve for the expected duration of the local anesthetic.
Results of Treatment
Injection of the piriformis may improve pain-related outcomes for several months. However, the published studies are limited by poor study methodology and reporting, inconsistent outcome selection, small sample sizes, heterogeneous patient populations, and the absence of standardized diagnostic criteria.
A retrospective study noted that 76% of patients treated with physical therapy and local anesthetic/steroid injection had greater than 50% improvement at an average 10.5-month follow-up. The combination of a sciatic nerve conduction study with the flexion, abduction, internal rotation (FAIR) test may predict those who will respond to physical therapy. A prospective study noted better outcomes with local anesthetic/steroid injection than with medication and physical therapy alone that were sustained for 1 year. Several uncontrolled studies have evaluated the use of botulinum toxin, often in combination with physical therapy, and reported high rates of success that lasted for months ( Table 64.1 ). A controlled study demonstrated superiority of botulinum toxin over placebo injection for 10 weeks. Other controlled studies have reported that the efficacy of botulinum toxin is superior to that of local anesthetic/steroid or normal saline injections for the treatment of piriformis syndrome when combined with physical therapy. One study found good results using clonidine.
