TRIGGER POINT INJECTIONS:
NEURAL BLOCKADE FOR THE TREATMENT OF MUSCLE TENSION AND CERVICOGENIC HEADACHES
1. Use of Trigger Point Injections by the Practicing Physician
2. Use of Occipital Nerve Blocks by the Anesthesiologist
3. Use of Manipulation and Acupuncture by the Neurologist
4. Use of Acupressure, Massage and Manipulation by the Physical Therapist
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The medical use of trigger point injections started thousands of year ago with the Chinese and others in the far East. Someone, thousands of years in the past, determined that pressure over certain spots on the body had effects at distant locations. These pressure points, led to the development of multiple forms of medical practice considered alternative in our Western society: acupuncture, Renke, Roulfing, Reflexology, Massage, Manipulation (Chiropractic) etc.
All these modalities are based in fact: they work. The science has been slow in coming and the Western Medical Concept of prescriptions and surgery are more invasive, more permanent, and have more complications. Whenever a simple, safe, alternative methodology can treat or ‘cure’ a problem, it is better for the patient. Always.
WHAT ARE TRIGGER POINTS
Trigger points are locations in muscles where a knot or whorl has developed. The body may be producing this swollen, knotty muscle whorl in an effort to either protect the nerve in this location as a response to local nerve irritation. Most typical locations for these ‘knots’ are:
OCCIPITAL at the top of the spinal muscles that run up to the skull, approximately one inch off the midline (Cervical Root C2)
CERVICAL about 2/3rds down the neck approximately 1- 1 1/2 inches off the midline (Cervical Root C4-5)
SHOULDER deep behind the scapula
LUMBAR-SACRAL: locations 1/2 to1 inch off the midline at the curvature of the lower back (Lumbar 1 through 4)
SCIATIC: deep in the buttock about 4 inches from the midline
An excellent source which describes trigger points in more detail is the book by Janet Travell, M.D. and David Simon, M.D.; Myofascial Pain and Dysfunction, The Trigger Point Manual. First Edition 1983; second volume 1994.
USES AND INDICATIONS
The treatment of headache is the most common application of Trigger Point Injections. Trigger point injections can be used for both migraine and tension type headaches. Their use in the Emergency Room would save hundreds of millions of dollars since they would eliminate the need for most MRI and CT scan. The failure of these blocks are an indication that something non-muscular is amiss: broken necks, strokes, infections in the jaw, ear or teeth, for example, will not respond to Trigger Point Injections.
MIGRAINE: The headache is one of the most common complaints encountered by physicians of all specialties. Headache is a complaint in more than half of all physician visits and is the seventh leading complaint at ambulatory medical centers in the United States. Furthermore, it is frequently disabling. Five to ten percent of young adults report missing at least a part of a day’s work each month as a result of headaches. Consequently, the physician faces a major task in addressing patient’s headache complaints. Fortunately, this task is simplified by the fact that 90% of all headaches are classified as muscle tension headaches. Only about 6% are migraine or a variant of migraine headaches while the remainder fall into the mixed or rare categories. [Dobritt]
TENSION TYPE HEADACHE: Patients who suffer from muscle tension headaches usually complain of continuous, dull, deep, non-throbbing ache, tightness or pressure sensation in the cervical, occipital, frontal or temporal areas. Symptoms are unilateral in approximately half of the patients and bilateral or changing in the remainder. The headaches typically have a gradual onset, last a few hours to several days and gradually terminate. Patient’s often relate the onset of headaches to stress, depression, worry, anxiety or alcohol consumption. Patients deny associated gastrointestinal, nasal, visual or neurological symptoms and there usually is no family history of similar headaches. The physical examination is generally negative with the possible exception of tenderness and myofascial trigger points of muscle insertions in the area of the headache. Laboratory studies are usually negative and rarely helpful. Patients with muscle tension headaches are typically adults, but may be of any age. Women are more likely to suffer from muscle tension headaches then are men. Many patients tend to be conscientious, nervous, unable to relax, or described as high-strung, and some are anorexic. However, the symptoms, signs and associated personality trait of the muscle tension headache are variable. [Dobritt]
Muscle tension headache, never-the-less, is quite unlike the throbbing hemicranial [half of head] vascular headache with associated gastrointestinal or visual symptoms. Acute headaches are associated with glaucoma, purulent sinusitis, meningitis, a subarachnoid hemorrhage [intracranial bleed] and chronic unrelenting headaches with space occupying tumors and cysts with associated papilledema [swollen back of eyes] and neurological symptoms. Some persons seem to have inherited poor muscle control, and since childhood have a tendency to develop tenderness not only of the muscles in the head but of muscles in other parts of the body as well. This tendency is often associated with an anxious constitution. In other patients actual conflict problems or working conditions seem responsible. In each patient the relative importance of the many factors listed should be estimated. [Dobritt]
HOW TO DO TRIGGER POINT INJECTIONS
The physician identifies the tender location and possibly the knot in the muscle at the locations previously described. Patients have been known to put small hard balls or the have a partner rub and massage these knots in an attempt to ‘rub them out.’ When all else fails, a physician can needle these knots (acupuncture) or inject a solution again with the attempt to make these painful knots dissolve (i.e. disappear).
Travell and others used either normal saline (salt water) or, as I prefer, a mixture of local anesthetic agents and an anti-inflammatory medication. My formulation is in a 10cc syringe: 5cc of 1% xylocaine (lidocaine), 4cc of .025% Marcaine (bupivacaine) and 1/2cc of dexamethasone (1 mg).
The location of the trigger point is palpated. When the location is confirmed, The syringe with a 1 inch 25 gauge needle is positions at a 90degree angle to the skin surface. When the needle enters the ‘trigger point’ knot of muscle, the patient will ‘jump’ or ‘twitch.’ This is called the ‘jump sign’ and denotes that the needle is in the correct position.
The physician then injects a small amount of medication while retracting the needle through the muscle. This is repeated in multiple directions so that a stellate (star-like) block is performed covering approximately 1 square inch of deep muscle. the procedure is usually repeated on the opposite side.
Relief is almost instantaneous. The patient has not only relief of pain but also an increased range of motion for the neck in flexion and rotation and in the shoulder with range of motion of the shoulder in a circular (clock-wise motion) and also in the front to back direction.
Sciatic block is associated with increased flexion: the individual can more likely flex toward touching their toes without pain.
AGAIN NOTE: the failure to relieve pain should make the physician more aware that further evaluation for other modalities should be considered.
MORE INFORMATION ABOUT TRIGGER POINTS from Dr. Dobitt PRESENTATION
A relatively simple patho-physiological model for tension headache has been widely accepted, but the picture is now becoming more complex. It was thought that involuntary over-activity of pericranial muscles compressed small blood vessels creating ischemia of the extra cranial muscles. Pain was thought to be at least in part due to ischemia. Multiple electromyographic studies have recorded surface potentials over pericranial muscles in patients with tension headache and migraine in abnormal controls. Although muscle activity is probably increased in patients with tension headache, the increase is modest and in many patients it is absent. In fact, migraine patients display a greater level of increased muscular activity. Because it would take a fairly m arked tonic contraction to cut off blood supply, however, the ischemic hypothesis has been thrown into doubt. It is possible that low grade long lasting tonic contraction of muscles could by unknown mechanisms cause muscle fatigue, tender spots and pain. The majority of patients with tension headache are more tender on palpation than normal people, although some are not. Tender spots, also called trigger points, in muscles might thus be the source of pain in most patients, but in others the source of pain is unknown. Psychological abnormalities have been found in many studies in which psychiatric aspects of tension headache have been examined. The most prominent features are anxiety, depression and repressed anger. Some abnormalities are known to be a consequence of prolonged pain and suffering and can enhance transmission and nociceptive information. Recently it has been shown that beta endorphins in the spinal fluid is decreased in patients with chronic tension headache. This finding suggests a decreased tone in the anti-nociceptive system. It is possible that in these patients there is an inter-relationship and/or potentiation of the psychological factors and a facilitated nocicpetive system.
In the future it will probably become possible to split tension headache into two, or perhaps even several diagnostic entities. Today the diagnosis is similar to that of unspecified anemia. We are unfortunately forced to live with this poorly defined d iagnosis until further research clarifies matters.
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Tension headache is an ill defined pain syndrome. In fact, the name itself has been disputed and is not included in the classification proposed by the Ethic Committee of the National Institutes of Health which used the tern “muscle contraction headache." Where as tension can refer both to psychological tension and increased tone of pericranial muscles, muscle contraction headache refers only to the latter. In Europe the term cephalgia psychomyogenica is often used implicating both the mind and the muscles. The widely accepted definition proposed by the Committee of the National Institutes of Health is imprecise and non-operational. The new classification includes several types; episodic tension type headache, chronic tension type headache and unclassified tension headache-like disorders. The episodic tension type headache can be associated with increased tenderness and electromyographic evidence of pericranial muscle dysfunction in which case it is called episodic muscle contraction headache. If it is not associated with pericranial muscle dysfunction, it is called chronic idiopathic headache. The most common form is the episodic type of headache with and without pericranial dysfunction.
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The cervical spine and associated muscular support of the head interwoven with vessels and nerve supply in the head and upper extremities, compose a complex structure with many sites for the generation of pain. A reduction in the space in which nerves pa ss through or lie can result in pain and loss of function. If the pressure is acute, pain is more likely to occur. Loss of function is generally the result of more prolonged and continuous pressure.
The sites of nerve compression in the neck are the intervertebral foramina, the spinal canal, the interscalene space and the course of the occipital nerves through the trapezius muscle at the base of the skull. Impairment or free movement at the joints, discs or ligaments may lead to irritation of sensitive structures of the joints and soft tissue of the neck. Reflex muscle spasms resulting from this irritation can produce continuous tension on the periosteal insertion of muscles. It is common for head and neck pain to originate with stress on the cervical musculature. Tension headaches are the result of sustained muscle contraction which produces both irritation at muscle insertion points and ischemic pain of the muscle itself.
Irritation of the cervical nerve roots at any point from their origin of the spinal cord to their paths to the occipital muscles can result in pain referred to the head and neck or upper extremity. Common sources of such irritation are the degenerative changes associated with osteophytes. As the degenerative process progresses, the spinal canal decreases in all diameters causing pressure on the long ascending and descending tracts as well as the cervical nerve roots. The most frequent complaint of the patient with cervical spondylosis is cervical, occipital or atypical facial pain due to irritation of the C2, C3 and C4 nerve roots. The continued irritation of these roots as they exit from the intervertebral foramina produce an inflammatory response i n the root with secondary edema.
As the greater and lesser occipital nerves pierce the trapezius at the base of the skull they are subject to pressure by cervical muscles and spasm. The result, an occipital neuralgia, produces further cervical spasms leading to a reflex perpetuation of occipital pain. Carcinoma and tumor invasion of the cervical spine and soft tissues of the neck may cause destruction as well as encroachment in cervical nerve roots or invasion of branches of the cervical plexus. These malignant forms of cervicogenic headache will not be discussed.
The purpose of this discussion is to describe those injection techniques that have been found useful in the treatment of muscle tension and cervicogenic headaches. These procedures include: trigger point injections, occipital nerve blocks, anesthetic blocks of the cervical nerve C2-C5, facet joint blocks at C2, C3 and cervical epidural steroid injections.
TRIGGER POINT INJECTIONS
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A myofascial trigger point is a hyperirritable locus within a taut band of skeletal muscle located in the muscular tissue and/or its associated fascia. The spot is painful on compression and can evoke characteristic referred pain and autonomic phenomena. A myofascial trigger point is to be distinguished from a trigger point in other tissues such as skin, ligament and periosteum. Myofascial trigger points can be furthered classified into active and latent. Active trigger points cause the patient pain a nd a latent trigger point is clinically silent with respect to pain, but may cause restriction of movement and weakness of the affected muscle. A latent trigger point may persist for years after apparent recovery from injury. It is predisposed to acute attacks of pain since minor overstretching, overuse or chilling of the muscle may suffice to reactivate it. Both latent and active trigger points cause dysfunction, but only active trigger points cause pain.
Myofascial pain is referred from trigger points in specific patterns characteristic of each muscle. The spontaneous pain is rarely located at the trigger point responsible for it. The referred pain of myofascial trigger points usually is dull and aching and often deep with intensity varying from low grade discomfort to severe and incapacitating torture. It may occur at rest or only on motion. The referred pain can usually be elicited or increased in intensity by digital pressure on the trigger point or by perpetuating the trigger point precisely with a needle. The more hypersensitive the trigger point the more intense and constant is the referred pain and the more extensive its distribution.
There is a multitude of muscles which may refer pain to specific areas of the head and neck resulting in headaches. These include the muscles of mastication, sternocleidomastoid, occipitalis, trapezius and cervical paraspinal muscles. An excellent source which describes trigger points in more detail is the book by Janet Travell, M.D. and David Simon, M.D.; Myofascial Pain and Dysfunction, The Trigger Point Manual.
Histologically, trigger points contain large quantities of platelets and mass cells, fine fat deposits, abnormal vascular and mitochondria, serous exudates and mucopolysaccharide deposits. Physiologically, such trigger points are tonically contracted mu scle with impaired circulation. Clinically, they are identified as exquisitely tender points within palpable tight ropey nodular bands of muscle and spasm. When trigger points are spontaneously active or when firm finger grip pressure is applied to them , muscle spasm, pain, tenderness and autonomic changes including vasodilatation and pilomotor reaction are referred to sites that correspond to a characteristic muscle distribution rather than to nerve distribution. Once identified, a small gauge needle, usually 25 to 27 gauge, is inserted directly into the trigger point where a small dose of 1-2 cc of local anesthetic is injected into the muscle. Some authorities advocate the use of corticosteroids with injection of local anesthetic. If the needle is pl aced properly, the muscle will react with an involuntary twitch response, or the patient may grunt or moan, called the jump sign, when the needle impales the trigger point. The local referred tenderness will be intensified as the anesthetic is injected a nd the patient will frequently thereafter report some relief of local myofascial pain and associated headache. This objective reduction of muscle spasm response to trigger point injections has been documented by objective electrophysiologic testing. To achieve the goal of “breaking up" the trigger point to thereby relieve muscle spasm associated headache, injections repeated every few days may be necessary.
OCCIPITAL NERVE BLOCKS
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To understand how a blockade of the occipital nerve is efficacious in the treatment of headache, a review of the anatomy will be presented. The greater and lesser occipital nerves are sensory nerve which enter into the second, and to some extent the thir d cervical segments. The nerves enter the spinal cord via the Tract of Lissauer to terminate in the substantia gelatenosa of the upper cervical cord where they synapse. The infratentorial intracranial structures are innervated by the upper three cervical nerves. Sensory cutaneous distribution in the occipital nerve is over the back of the head anteriorly to the borders of the innervation of the first division of the trigeminal nerve. The C2 component is a more medial band extending form the superior nuchal line to this boundary. C1, when present, innervates an overlapping area more posteriorly. The greater occipital nerve passes over the superior nuchal line midway between the mastoid process on the occipital protuberance just lateral to the insertion of the nuchal ligaments. The lesser occipital protuberance is just lateal to the insertion of the nuchal ligaments. The lesser occipital nerve passes laterally to the greater occipital nerve over the nuchal ridge.
The greater occipital nerve runs transversely and then turns at right angles to run posteriorly. It then emerges through the aperture above the aponeurotic sling between the trapezius and the sternomastoid. This fact renders untenable any speculation that it may be compressed by spasm in the trapezius. Similarly, the nerve is not vulnerable to bony compression between the posterior arch of the atlas and the lamina of the axis. How the occipital nerve becomes sensitive to the diverse headache condition described is still a matter of speculation.
Occipital nerve blockade has been used for the treatment of diverse headaches for decades. The most effective position for greater occipital blockade is sitting or lateral decubitus with the chin flexed upon the chest. A short 25 gauge needle is inserted through the skin at the level of the superior nuchal line so as to develop a wall of local anesthetic surrounding the posterior occipital artery. The procedure should be done under strict aseptic conditions. The artery is commonly found approximately o ne-third of the distance between the external occipital protuberance and the mastoid process on the superior nuchal line. Injection of 3-5 ml of local anesthetic in this area with or without depo-corticosteroids will produce satisfactory anesthesia. Due to the superficial nature of this block complications are infrequent but may include hematoma, infection and paresthesia. Occipital nerve blockade will local anesthetic may also be used as a prognostic tool to determine if rhizotomy is warranted in refr actory cases. Occipital rhizotomy may be performed surgically or using a cryoprobe.
C2/C3 Facet Joint Blockade
The intimate relationship between the trigeminal nucleus and the ascending fibers in the brain stem originating from the C2 and C2 level may explain why cervical processes may cause pain in the forehead. Recent observations suggest, however, that headac he may arise from lesions in lower cervical levels. The C6-C7 lesions are often clinically detectable, (e.g. reflex anomalies, pain radiating to the fingers) and C5 lesions may partly influence the biceps reflex. On the other hand C2-C4 lesions may be difficult to detect on neurological examination. The facet joint C2/C3 may be vulnerable to neck trauma, since it represents a functional transition zone between the segment of rotation above it and the segment of flexion/ extension underneath it. The joint receives innervating fibers mainly from the C3 dorsal ramus (third occipital nerve), but also from the C2 dorsal rami. There are, however, some variations in the innervation especially regarding the fibers from C2. The third occipital nerve has a clos e relation to the C2-C3 facet joint capsule. Peripherally it conveys sensory fibers to the skin.
Blockade of the second cervical nerve root should be carried out with the use of X-ray fluoroscopy. The transverse process of C2 is identified and 1cc of local anesthetic is used to anesthetize the skin under strict sterile conditions approximately 1.5 c m below the mastoid process and 1.5 cm lateral to the spinous process. A 22 gauge Teflon coated nerve stimulating needle attached to a constant current nerve stimulator is inserted in a slightly caudal direction. The needle tip is advanced until a twitc h response is noted over the second cervical nerve root. The needle tip is repositioned until the twitch response is maximized at .5 milliamps. At this point 1.5 ml of local anesthetic in injected.
Injection into the facet joint C2/C3 is monitored by fluoroscopy. Patients are positioned on their non-symptomatic side. The C2-C3 level is identified using fluoroscopy. One cc of 1% Xylocaine is used to anesthetize the skin approximately 1.5 cm later al to the spinous process at the level of the C2/C3 facet joint. Next, a 22 gauge 2 inch needle is inserted until bone is contracted. The needle tip is relocated until it is positioned at the C2/C3 facet. The needle tip is verified using fluoroscopy in the AP and lateral views by introduction of contrast medium. Next, 1-2 cc of local anesthetic with depo-steroids is injected. In refractory cases, diagnostic C2/C3 facet blockade with local anesthetic may be used to determine if facet rhizotomy using cryoanalgesia is indicated.
Cervical Epidural Steroid Injection
Unfortunately, many patients do not respond to the above mentioned injection procedures. Cronen, et. al., has reported good results with cervical epidural steroid injections in patients who are refractory to more traditional modalities. This makes sense when one considers the etiology of tension headaches may be secondary to cervical spinal pathology. Interestingly, there is little correlation between the degree of cervical spine abnormality such as degenerative disc disease or spondylosis seen on plain radiographs and the presence, duration and/or intensity of cervicogenic or tension type headaches.
Cronen’s study was conducted in the outpatient setting. The initial cervical epidural steroid injection contained 80 mg of depo-methylprednisolone and 7 ml of 0.25% preservative free bupivicaine. Subsequent blocks were administered on an every other day basis with 40 mg of depo-methylprednisolone and 7 ml of 0.25% preservative free bupivicaine in each nerve block. Up to six blocks per patient were administered with the end point being complete relief of pain. The average number of nerve blocks per patient necessary to obtain complete pain relief was four. Significant relief of pain was noted by the majority of patients at 3 months follow-up. Subsequent studies have confirmed the safety of this technique in the symptomatic relief of a variety of painful conditions of the cervical spine. The authors concluded that cervical epidural steroid injections may be utilized early in the course of a treatment program while awaiting for antidepressant medication and other modalities to become effective.
In conclusion neural blockade with local anesthetic may be useful as a diagnostic procedure to identify pain pathways and to aid in the diagnosis of the origin and sit of headache pain. Neural blockade with local anesthetics may also be used in a prognostic manner to predict the effects of the destruction of a given nerve. Therapeutic nerve blocks with local anesthetic and steroids can be useful in relieving a variety of painful conditions of the head including tension type headache. However, neural blockade should not be used as a single modality for the treatment of tension type or cervicogenic headaches, but rather intelligently integrated into a comprehensive treatment program.
- Hendler N, Kozikowski JG, Schlesinger R, Schlesing J. Diagnosis and Treatment of Muscle Tension Headaches. Pain Management 1991, April/May, 33-41.
- The Management of Pain. JJ Bonica, ed. Second edition. Lee and Febiger, Philadelphia and London, 1990, Vol. 1 Chapter 7, pg. 11-16.
- Carron H. Control of Pain in the Head and Neck. Otolaryngologic Clinics in North America 1991; 14(3): 6:31- 6:51.
- Gawel MJ, Rothbart PJ. Occipital Nerve Block and the Management of Headache and Cervical Pain. Cephalagia 1992;12:9-13.
- Bovim G, Berg R, Dale LG. Cervicogenic Headache; Anesthetic Blockades of Cervical Nerves C2-C5 and Facet Joints C2/C3. Pain 1992;49:315-320.
- Cronen MC, Waldman SD. Cervical Steroid Epidural Nerve Blocks in the Palliation of Pain Secondary to Intractable Tension Type Headaches. Journal of Pain and Symptom Management 1990;5(6); 379-381.
- Travell J, Simon D. Myofascial Pain and Dysfunction, The Trigger Point Manual. (Williams & Wilkins, Baltimore), 1983.
Revised: January 1, 2011