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INTRODUCTION
Chronic forearm pain disrupts daily life, including brushing teeth, face washing, eating food, or opening doors. One of the most common sources of forearm pain is considered to be tennis elbow (lateral epicondylitis) or golf elbow (medial epicondylitis). If the pain is localized to the lateral forearm and tenderness is localized on the lateral epicondyle, tennis elbow is suspected.
However, a hidden, underdiagnosed brachioradialis (BR) muscle contraction should be considered an important source of the forearm pain even though the prevalence is not proven. A prolonged, excessive contraction of the BR muscle elicits pain and tenderness of the lateral forearm from the lateral surface of distal humerus above the lateral epicondyle (its origin), through the BR muscle belly, to the styloid process of the radius (its insertion) [1].
Differential diagnosis with common disorders is needed from the origin, muscle belly, and insertion. First of all, lateral epicondylitis can be differentiated due to its different origin, the lateral epicondyle. Second, the common source of forearm pain from the lateral elbow to the muscle belly is radial tunnel syndrome (RTS). Third, numbness or pain on the thumb needs differential diagnosis from de Quervain’s tenosynovitis [2]. In addition, other disorders which provoke pain in the thumb are carpal tunnel syndrome (CTS), trigger thumb, and writer’s cramp. Fourth, cervical radiculopathy, especially in the C6, also shows numbness of the thumb and/or index finger [3].
In patients with subacromial bursitis due to repeated overhead movement in sports, such as golf, tennis, swimming [4], volleyball [5] or baseball, BR muscle contraction is commonly observed in the clinical field.
Efforts to search 286 scientific articles in PubMed to find clinical criteria or diagnostic measures for prolonged and excessive BR muscle contraction and pain came to nothing. This brief review describes the anatomy and function of the BR muscle, pathophysiology and diagnosis, differential diagnosis, commonly combined disorders, and treatment of BR muscle pain.
MAIN BODY
1. Anatomy and function of the BR muscle
The forearm muscles can be divided into three groups: the flexors, extensors, and radialis muscles. The radialis muscles are composed of the BR, extensor carpi radials longus (ECRL), and extensor carpi radials brevis (ECRB) muscles [1].
The BR muscle arises from the lateral surface of the distal humerus and lateral intermuscular septum which is a connective tissue wall that separates the upper arm into the anterior (the biceps brachii and brachialis muscles) and posterior compartment (the triceps muscle). The BR, ECRL, and ECRB muscles of the radialis muscles originate from the lateral distal humeral shaft, lateral supracondylar ridge, and lateral epicondyle of the humerus, respectively. The BR muscle inserts into the styloid process of the radius. However, the ECRL and ECRB muscles insert into the dorsal base of the second and third proximal metacarpal bones over the wrist joint, respectively. Therefore, the BR muscle contracts the elbow to flex and to slightly pronate the radioulnar joint. The BR muscle acts as a consistent elbow stabilizer during elbow flexion as a primary function and as a pronator rather than supinator during rotation [6]. However, the ECRL and ECRB allow the elbow to slightly flex and the wrist joint to extend dorsally (assists in fist closure) and to abduct (radial deviation). These muscles are innervated from the radial nerve from C5 and C6, C6 and C7, and C7 and C8, respectively (Fig. 1) [1].
2. Pathophysiology and diagnosis of BR muscle spasms as a myofascial pain syndrome
The BR muscle easily develops myofascial pain syndrome, resulting from repetitive microtrauma to the muscle from various activities, including work, sports for weekend athletes, and housework.
The pathognomonic lesion of the BR muscle spasms and contracture is the trigger point on the BR muscle belly which shows a point of sensitive tenderness. This can best be demonstrated in a flexion and pronation of the forearm against active resistance. In addition, point tenderness also commonly presents over the lateral distal humeral shaft proximal to the lateral epicondyle at the origin and less often presents over the styloid process of the radius at the insertion. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. Jump sign, involuntary withdrawal of the stimulated muscle, is also noted over the BR muscle belly and origin/insertion. Taut bands of muscle fibers are often identified when myofascial trigger points are palpated [7].
Histologically from the biopsy, the BR muscle hosting the trigger points is described either as “moth-eaten” or as containing “waxy degeneration.” Electrodiagnostic testing may reveal an increase in muscle tension [7].
BR muscle spasms exhibit a diagnosis of exclusion, reached by a process of elimination. Therefore, differential diagnosis of prolonged and excessive BR muscle contraction is needed according to pain at the belly, origin, and insertion of the BR muscle because its referred pain can mimic other painful disorders. In addition, a prolonged and excess BR muscle spasm may be combined with or secondary to various other musculoskeletal disorders.
3. Differential diagnosis from the site of pain or tenderness
1) Pain in the lateral elbow: lateral epicondylitis
Thorough physical examination, especially tenderness on the origins of BR and ECRB muscles, reveals BR muscle contraction without lateral epicondylitis. Lateral epicondylitis is the most common cause of lateral elbow pain. However, a misdiagnosis of lateral epicondylitis can sometimes occur in patients with posterolateral elbow stability, radial nerve compression, inflammatory osteoarthritis, osteochondritis dissecans, posterolateral plica, and primary osteoarthritis [8].
Lateral epicondylitis is very common (0.4%–0.7% of incidence and 1%–3% of prevalence yearly) and is frequent during the fourth and fifth decades of life (peak between the ages of 45 and 54 years) without gender difference [9]. It commonly occurs due to repetitive occupational (using vibrating tools) or athletic activities involving the wrist extension and supination. It is commonly referred to as tennis elbow, with a 10% (1 year) and 50% (lifetime) prevalence of those who play tennis affected. The incidence is higher in those who perform the one-handed backhand stroke. In patients with lateral epicondylitis, a trigger point was noted in the BR (82.5%), biceps brachii (55.0%), triceps brachii (27.5%), ECRB (20.0%), and supinator (2.5%) muscles, in order of frequency [9-11].
Pain is mainly located at the lateral epicondyle, extending along the extensor muscles, and aggravated by wrist and finger extension against resistance. Natural history is generally self-limiting within 2 years, with complete resolution for 90% within 1 year. Pain is exacerbated by lifting or holding activities in pronation [9].
The lateral epicondyle of the humerus becomes the common origin of the wrist extensor muscles, including extensor digitorum communis, extensor digiti minimi, extensor carpi ulnaris muscles of the superficial extensors of the wrist and the supinator muscle of the deep extensors. The ECRB of the radialis muscles shares the lateral epicondyle as an origin. The lateral epicondyle also attaches the lateral collateral ligament, annular ligament, and intermuscular septum [1,9,10].
A gross appearance shows grayish, shiny, edematous, and friable immature scar tissue; histologic features include angiofibroblastic hyperplasia in collagen microstructure, hyaline degeneration, and calcific debris [11].
Provocation tests include Maudsley’s and Cozen’s tests. In the Maudsley’s test, a patient is instructed to sit with their elbow flexed at 90° and forearm pronated. Then the patient extends their middle finger against resistance. In the Cozen’s test, a patient stands with the affected elbow fully extended and forearm pronated. The examiner places his/her thumb over the lateral epicondyle and asks the patient to clench their fist and extend, pronate, and radially deviate their wrist against resistance. Based on anatomic attachment of the ECRB, physical examination on an extended elbow reveals reproduction of pain with resisted middle finger and wrist extension. Grip strength may be diminished due to pain. Therefore, the “chair test” elicits lateral elbow pain on lifting a chair with a pronated hand [9,12].
Imaging tools include plain radiography, ultrasonography, and magnetic resonance imaging (MRI). In the presence of limitation of motion, crepitus, or a loose body, anteroposterior, lateral, and radiocapitellar plain radiologic views are recommended. Ultrasonography or MRI shows thickening, hypoechogenicity, or defects in the teno-osseous enthesis [12,13].
Differential diagnosis of lateral elbow pain includes cervical radiculopathy, RTS, an intra-articular loose body, chondral lesions, tumor, avascular necrosis, or osteochondritis dissecans [10].
Injection with steroids, whole blood, or platelet-rich plasma is introduced 1 cm distal and 1 cm anterior to the lateral epicondyle. Botulinum toxin is introduced into the ECRB muscle [12].
2) Proximal lateral forearm pain: RTS
Tenderness on the proximal belly of the BR muscle and pain/numbness in the RT should be differentiated. RTS is an entrapment neuropathy which is a symptom and sign constellation (chronic aching pain of the lateral and dorsal forearm) caused by compression of the posterior interosseous nerve (PIN, the motor terminal of the radial nerve), a deep branch of the radial nerve. Radial nerve compression at the elbow (especially, PIN compression) is the third most common compressive neuropathy of the upper extremity after CTS and cubital tunnel syndrome [14].
The radial nerve splits into the superficial branch and deep PIN, 3–4 cm distal to the lateral epicondyle under the BR muscle within the RT. The RT is musculoaponeurotic furrow which extends from the lateral epicondyle to the distal edge of the supinator muscle. However, the arcade of Fröhse (supinator arch) is a fibrous arch which is the superficial head of the supinator muscle and becomes the most common site of compression of the motor branch of the radial nerve [15].
The radial tunnel is a potential space which is bound on the lateral side by the BR, ECRL, and ECRB muscles and on the medial side by the biceps brachii and brachialis muscles. Its floor is formed by the capsule of radiocapitellar joint [16]. Therefore, five possible offenders of RTS include: (1) the fibrous adhesions between the brachialis and BR muscles; (2) the leash of Henry (the vascular arcades of the radial recurrent vessels); (3) the fibrous edge of the ECRB; (4) the arcade of Fröhse; and (5) fibrous bands associated with the supinator muscle [17]. The most common compressive site is the arcade of Fröhse (46%). It is a supinator arch which is the most superficial layer of the supinator muscle and becomes a fibrous arch of the PIN [18].
The rule-of-nine test is helpful to consider RTS. A large square box over the anterior aspect of the proximal forearm in a fully extended elbow and fully supinated forearm position is divided into 9 smaller equal squares. The PIN travels through the lateral column; the median nerve travels through the medial column; nothing travels through the middle column. Other clinical tests for RTS include the middle finger extension test, resisted supination of the forearm, and a local anesthetic RT block [19].
Only 5.7% of the patients with RTS had a diagnosis of lateral epicondylitis on the same side within 6 months of RTS diagnosis [20].
3) Pain in the wrist and hand
Referred pain from the insertion site (styloid process) of the BR contraction muscle should be differentiated from painful disorders in the wrist and hand.
(1) De Quervain’s tenosynovitis
De Quervain’s disease is stenosing tenosynovitis of the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons, which control the movement of the thumb in the first compartment of the six dorsal extensor compartments of the wrist [9]. Pain is located on the lateral side of the wrist and/or distal forearm. It is caused by synovial sheath inflammation and chronic myxoid degeneration of the fibro-osseous sheath, as well as by somatotropin exposure and genetic propensity [22].
The first dorsal compartment includes the APL and EPB tendons, which insert on the metacarpal bone and middle phalanx of the thumb, respectively. Different insertion sites may result in different gliding resistances or friction coefficients, developing stenosing tenosynovitis. Patients with de Quervain’s disease have one APL and one EPB tendon slip; normal cadavers show two APL and one EPB tendon slips [23].
Pain is located at the region of the radial styloid process during activity such as wrist and thumb movement. De Quervain’s tenosynovitis is common in women between the ages of 30 and 50 years. It occurs more frequently during pregnancy or breastfeeding due to generalized edema. Risk factors in pregnancy-related de Quervain’s tenosynovitis include increased age (≥ 30), multiple gestation, cesarean section, hypertensive or diabetic disorders related to pregnancy, and rheumatoid arthritis [23]. It is more prevalent in those who engage in repetitive hand and wrist movements, such as typing, knitting, gardening, and playing golf and tennis [24].
The most common clinical diagnostic modalities include the Finkelstein and Eichhoff tests. The Finkelstein test involves the examiner holding the patient’s thumb firmly with one hand while applying firm traction longitudinally and in the direction of slight deviation to the wrist with the other hand. On the other hand, the Eichhoff test requires the patient to oppose the thumb into the palm and clench the fingers while the examiner passively applies ulnar deviation to the wrist. In addition, the wrist hyperflexion and abduction of the thumb (WHAT) test requires the patient to actively hyperflex the wrist and abduct their thumb as the examiner’s index finger provides counter pressure. Specificity and sensitivity in the order of higher probability are known to be the WHAT, Finkelstein, and Eichhoff tests [22].
Ultrasound is the most common imaging modality in clinical practice. It can identify the sizes and presence of a hypoechoic septum between the APL and EPB tendons, as well as intratendinous degeneration and synovial proliferation [23]. MRI shows increased APL and EPB tendon thickness and peritendinous edema rather than surrounding subcutaneous edema or increased signal within the tendon [23,25].
Ultrasound-guided steroid injections have similar results for disability scales, patient-reported outcome measures, and pain scores, compared with surgical release [26].
(2) CTS
CTS is characterized by numbness and tingling in the thumb, index, middle, and ring fingers and by weakness of thumb opposition in severe cases due to compression of the median nerve under the transverse carpal ligament of the wrist (carpal tunnel). The median nerve is in charge of sensation of the thumb, index, and middle, and radial half of the ring finger and motor function for wrist and finger flexion and thumb opposition. Progressive median nerve compression shows ischemic change, blood-nerve barrier breakdown, perineural edema, focal demyelination, and finally axonal loss. CTS is caused by local (trauma or tumor) and systemic (pregnancy, obesity, diabetes, hypothyroidism, or amyloidosis) factors. It frequently occurs in the female sex, those aged 41 to 60 years, obese people with body mass index > 30 kg/m2, and diabetes, as well as in those performing repetitive tasks (computer or mouse use). It is the most common peripheral nerve entrapment in the upper extremity [30,31].
The carpal tunnel is an opening formed by the carpal bones on the bottom of the wrist and the transverse carpal ligament (flexor retinaculum) across of the top of the wrist. It contains the median nerve and tendons of flexor carpi radialis, 4 flexor digitorum superficialis and 4 flexor digitorum profundus tendons, and the flexor pollicis longus (FPL) tendon. The flexor retinaculum bridges the carpal tunnel from the scaphoid over the lunate and triquetrum to the pisiform in the proximal row and from the trapezium over the trapezoid and capitate to the hook of the hamate in the distal row, from the radial to ulnar side (Fig. 2) [1,10].
The cause of CTS is supposed to be increased interstitial pressure (normal: 2–10 mmHg) within the carpal tunnel, resulting in compression and injury of the median nerve. Mechanical compression of the median nerve provokes ischemia, resulting in demyelination. Repetitive motions of the wrist create the increased interstitial pressure of the carpal tunnel, especially notable being 8 times and 10 times increase in wrist flexion and extension, respectively [32].
Typical symptoms include numbness, tingling, nocturnal paresthesia, and/or neurotic pins-and-needles pain in the radial 3.5 digits. Based on clinical symptoms, CTS can be divided into 3 stages. The first stage shows numbness and swelling-like sensation of the hand, brachialgia paresthetica nocturna, and flick sign (relief of pain after shaking of the hand). The second stage shows clumsiness in grasping an object. The third stage progresses to hypotrophy or atrophy of the thenar eminence and sensory loss [32].
Representative provocative tests include the Tinel sign and Phalen test. A positive Tinel sign is considered when repetitive tapping along the carpal tunnel produces symptoms in the same distribution of the median nerve. A positive Phalen test is pain provocation by letting the patient flex his/her wrist flex to 90°. The Phalen test shows high sensitivity and specificity, compared to the Tinel sign. In addition, the scratch test is performed by applying a light scratch over the skin of the compressed nerve while the patient resists rotating the shoulder externally. A positive scratch test is considered to be a transient loss of muscle resistance resulting in the arm collapsing [32].
The Boston carpal tunnel questionnaire is commonly applied to evaluate 11 items of the symptom severity scale (SSS) and 8 items of the functional status scale (FSS) of CTS (Table 2) [33]. The 11-item disability arm shoulder and hand (QUICK DASH) and its modified 9-item QUICK DASH (QUICK DASH-9) instead of the 30-item DASH are also helpful to evaluate disability and pain of the upper extremities (Table 3) [34].
Electrodiagnostic tests include nerve conduction studies (NCS) and electromyography (EMG). NCS detects impaired median nerve conduction across the carpal tunnel (median neuropathy at the wrist with normal conduction elsewhere). EMG reveals pathologic changes in the muscles innervated by the median nerve, typically the abductor pollicis brevis muscle. It allows severity of CTS, determination of demyelination versus axon loss, and ruling out coexisting disorders, such as cervical radiculopathy, polyneuropathy, brachial plexopathy, or proximal median neuropathy at the level of pronator teres muscle, thoracic outlet syndrome, stroke, or multiple sclerosis [32].
Ultrasonography reveals thickening of the median nerve, flattening of the nerve within the tunnel, and bowing of the flexor retinaculum. The cross-sectional area of the median nerve at the proximal entrance of the carpal tunnel is commonly observed: 7 mm2 to 10 mm2 in healthy controls, 10 mm2 to 13 mm2 in patients with mild symptom, 13 mm2 to 15 mm2 in patients with moderate symptom, and over 15 mm2 in patients with severe symptom [32,35].
MRI of the median nerve shows an ovoid structure of moderate signal intensity, which is distinguished from the flexor tendons. MRI also helps to evaluate space-occupying lesions which compress the median nerve, such as hemangioma, ganglion, or bony deformities [32].
Treatment includes conservative and surgical treatments. Representative conservative treatment is a corticosteroid injection for reducing inflammation and edema of the synovium and tendons. However, the injection may have a harmful effect on tenocyte by reducing collagen and proteoglycan synthesis, resulting in reduction of mechanical strength of the tendon and progression of degeneration [36].
Surgical treatments include endoscopic or open carpal tunnel release. Endoscopic carpal tunnel release has advantages, including decreased postoperative pain, earlier mobility and return to work, ability to perform the release of both hands simultaneously, minimal scarring of the median nerve, and decreased pillar pain, over open carpal tunnel release [35]. Ultrasound-guided percutaneous carpal tunnel release is also a very effective treatment with few complications [36,37]. While placing the ultrasonic probe at the level of the distal carpal tunnel (from the trapezium over the trapezoid and capitate to the hamate), a transverse safe zone should be found. The transverse safe zone is defined as a distance between the ulnar border of the median nerve (below the transverse carpal ligament) to the hook of the hamate or ulnar neurovascular bundle above the transverse carpal ligament. It means the space between the median nerve inside of the carpal tunnel and radial nerve and artery outside of the carpal tunnel (Fig. 2) [10,38].
Pillar pain is defined as a deep-seated postoperative pain over the thenar and/or hypothenar region and disappears after 6 months or is reduced over time [39]. It is supposed that the complication develops due to the dissection of the palmar cutaneous branch of the median nerve, dissection of free nerve endings in the transverse carpal ligament, and biomechanical disruption of the transverse carpal ligament, inflammation, or increased sympathetic tone [40].
(3) Trigger thumb
Trigger thumb is stenosing flexor tenosynovitis of the thumb, characterized by a narrowing of the flexor tendon sheath, especially thickening of the A1 pulley, resulting in pain and catching, clicking, or popping sensation during thumb extension. There are five annular ligaments and three cruciform ligaments in the other four fingers. However, the thumb has one oblique ligament between two annular ligaments over the FPL. The A1 pulley is located from the metacarpal bone through the metacarpophalangeal joint to the base of proximal phalanx. The oblique pulley attaches from the adductor pollicis brevis (APB) and flexor pollicis brevis (FPB) and covers the FPL between the A1 and A2 pulley. Both the extrinsic FPL and intrinsic FPB contribute to the flexion process (Fig. 3) [10].
Trigger thumb frequently occurs in overuse, especially repetitive gripping and flexion, and in systemic disorders, such as diabetes, amyloidosis, hypothyroidism, gout, and rheumatoid arthritis, resulting in hypertrophy and fibrocartilaginous metaplasia at the tendon-pully interface. Swelling and thickening of the tendon sometimes make Notta’s nodule, common in children.
The Quinnell grading system of trigger finger is divided into 5 grades according to mechanical symptoms: (1) grade 0: no mechanical symptoms without pain with flexion; (2) grade 1: uneven motion during flexion/clicking; (3) grade 2: locked digit that is actively corrected; (4) grade 3: locked digit that is passively corrected; and (5) grade 4: locked digit that is uncorrectable and fixed flexion contracture [41].
Treatment of trigger finger, including trigger thumb, includes noninvasive methods, injection techniques, and surgical methods. Noninvasive treatment includes activity modification, non-steroidal anti-inflammatory drugs for alleviating local inflammation secondary to triggering, and blocking splint of the metacarpophalangeal joint at 10° to 15° of flexion for 6 to 10 weeks for the limitation of tendon gliding to allow the time for inflammation to resolve [42].
Local steroid injections are very effective (50% to 70%); however, there is a high recurrence rate in younger age, type 1 diabetes mellitus, involvement of multiple digits, and history of other tendinopathies. The two common injection methods are palmar injection from proximal to distal direction and mid-axial needle trajectory injections. Extra-sheath rather than intra-sheath injection shows better outcome [42].
Open release of the A1 pulley is the golden standard for surgical treatment of trigger finger or thumb. It has a great success rate of over 99%. However, the complication rate is also high, ranging from 7% to 43%. Minor complications include superficial infection, wound dehiscence, persistent incision discomfort, and stiffness. The rare major complication in A1 pulley release for trigger thumb is digital nerve injury because of running the nerves over the A1 pulley. Accidental release of the A2 pulley in trigger finger leads to painful protrusion of the flexor tendon into the palm (flexor tendon bowstringing) and a decrease in flexion efficiency. Percutaneous A1 pulley release using a hooked knife under the ultrasonography also shows higher success rate of over 90% with few complications [42].
(4) Writer’s cramp
Writer’s cramp is a type of hand dystonia, showing an involuntary, sustained posture or contraction (flexion and extension) of the hand, fingers, and/or arm muscles during writing. It is the most common form of focal situational dystonia. Dystonia is referred to sustained or repetitive involuntary movements or abnormal fixed postures. It can be divided into focal (1 body part), segmental (2 or more contiguous body parts), multifocal (2 noncontiguous areas), hemidystonia, or generalized types. It is also divided into constant, intermittent, or situational (including task-specific) types. The pathophysiologic mechanism of dystonia is limited: basal ganglia abnormalities, lack of multilevel inhibition of the nervous system, increased neural plasticity, and abnormal sensory processing [43,44]. The BR reflex may be related to radial nerve entrapment, as seen in the scalene reflex related to brachial plexus entrapment [45]. It usually has an onset starting in adulthood and an insidious progression to around the 4th decade in men. Incidence is known to be 2.7/1,000,000 [44].
Writer’s cramp can be classified into simple (presentation only with writing), complex (symptom provocation by other similar tasks, including eating or shaving), or progressive (progression to the proximal extremity or unaffected limb without spontaneous remission). It is quite similar to musician’s focal hand dystonia, such as pianist’s or violinist’s cramp. Therefore, writer’s cramp or musician’s cramp, as well as sport-related problems, such as golfer’s yips, are called focal task-specific dystonia [43,46]. Writer’s cramp is usually focused on a coordination problem rather than pain due to overuse or repeated use while performing a specific task.
Treatment includes oral pharmacologic agents, such as anticonvulsants or skeletal muscle relaxants and botulinum toxin injection into the flexor digitorum superficialis, flexor carpi ulnaris, extensor carpi ulnaris, extensor carpi radialis, flexor digitorum profundus, FPL, flexor carpi radialis, pronator teres, extensor indicis, and extensor pollicis muscles, in order of frequency [47].
(5) Cervical radiculopathy
Cervical radiculopathy is defined as a complex of sensory (radicular pain), motor (difficulty in neck movement and muscle spasm or weakness), and/or reflex deficits (decreased triceps tenson reflex) due to compression or irritation of nerve roots in the cervical spine. It occurs frequently at the age of 50 to 54 years [3].
Clinical diagnostic tests include the Spurling test, shoulder abduction test, and upper limb tension test. Imaging diagnosis is required when the red flag signs appear. Electrodiagnosis is also necessary to rule out other upper extremity disorders or peripheral neuropathy [3]. Cervical radiculopathy should be differentiated from various regional pain disorders, such as referred pain from coexisting shoulder, wrist, and hand disorders through the history taking and physical examination.
Cervical radiculopathy is a self-limiting disease with 75% to 90% of patients receiving symptomatic conservative treatment. Conservative treatments include physical therapy, non-steroidal anti-inflammatory drugs, skeletal muscle relaxant, or epidural injection. Surgical options include anterior cervical discectomy and fusion, cervical disc arthroplasty, and posterior foraminotomy [3,48].
4. A common combined shoulder disorder, subacromial impingement syndrome, in patients with BR muscle pain
Subacromial impingement syndrome includes a spectrum from subacromial bursitis to rotator cuff tendinopathy, such as tendinosis or partial- and full-thickness tears. It comes from external compression (from the anterior acromion, coracoacromial ligament, and acromioclavicular joint), age-related degeneration, trauma, and vascular compromise.
The main symptom of subacromial impingement syndrome pain is limitation of motion that occurs when the patient lifts his/her arms overhead or reaches backwards. Pain and limitation of motion in the shoulder result in overuse and overexertion of the BR muscle, as well as extreme tightness and pain along the BR muscle belly in the forearm, elbow, and thumb [49].
Exacerbation of these symptoms is frequently reported by shoulder elevation at or over 90° or with lifting items away from the body. The Hawkins–Kennedy and Neer tests show high sensitivity (79% vs. 72%), but low specificity (59% vs. 60%), respectively [50]. The Hawkins–Kennedy test is a passive test in which an examiner flexes the sitting patient’s shoulder and elbow to 90°, supports the patient’s elbow with one hand and his/her wrist with the other hand, and finally internally rotates the patient’s arm. The test lets the contact between the acromion and humerus increase in order to provoke pain. The Neer test is also designed to reproduce the pain from subacromial impingement. An examiner stands behind the sitting patient and stabilizes the patient’s scapula with one hand. The examiner places the patient’s thumb down to internally rotate it and passively raises the patient’s arm to reproduce the pain [51].
A great merit of subacromial bursa injection through the acromioclavicular joint is that it can be injected into both the pathologic potential subacromial bursa and the degenerative acromioclavicular joint. Concomitant injections into the BR myofascial steroid injection and/or BR muscle botulinum injection should be given after the subacromial injection.
5. Treatment of the BR muscle pain
Conservative treatments include rest, ice, compression, and elevation (RICE). Limitation of use is recommended for at least 72 hours after the onset of the BR muscle pain. Ice for 20 minutes every 2 hours is recommended for preventing inflammation and swelling. Loose wrapping and elevation of the patient’s forearm can also decrease swelling. Exercise includes range-of-motion exercise (with bending the elbow and rotating the wrist performed by the patient) and isometric exercise (the patient holding the BR muscle for a set of time). Strength training can be started from lifting weights [49,52].
Pharmacologic treatment includes non-steroidal analgesics including non-steroidal anti-inflammatory drugs (effective only for acute stage, however, with adverse events occurring with chronic use) [53], opioids (only weak opioids for acute muscle pain, however, there will be negative results from use of strong opioids in occupational low back pain) [54,55], transdermal lidocaine patch/topical lidocaine (effective) [56-58], muscle relaxants including tizanidine (a centrally acting alpha-2-adrenergic agonist: effective) [59], benzodiazepines including clonazepam (which depress presynaptic release of serotonin and excite gamma-aminobutyric acid: effective) [60], and antidepressants (tricyclic antidepressants: effective, but duloxetine: no evidence). Therefore, a combination of analgesics (nonsteroidal anti-inflammatory drugs or weak opioids), muscle relaxant (tizanidine), antidepressants, and clonazepam may be helpful for the treatment of BR muscle spasm as a pharmacologic option [61].
Ultrasound-guided myofascial injection over the radius bone with a steroid and local anesthetic is helpful to reduce inflammation or irritation from ischemic events from a prolonged BR muscle contraction within 3 days. A prolonged BR muscle contraction needs intramuscular botulinum injection with a dose of 10–20 IU, based on strong evidence [62,63]. The symptomatic improvement of injected botulinum starts from 1 month and lasts for 6 months. Concomitant administration of myofascial steroid injection and intramuscular botulinum injection may expect both short-term and long-term therapeutic effects (Fig. 4).
CONCLUSIONS
There are few scientific articles related to painful persistent BR muscle contraction. BR muscle pain is very common, but underdiagnosed forearm disorder, especially in patients with subacromial bursitis.
For the diagnosis of BR muscle pain among other possible types of forearm pain, medial forearm pain disorders, including medial epicondylitis (golfer’s elbow) and cubital tunnel syndrome in the elbow/Guyon’s canal syndrome in the wrist, due to ulnar nerve entrapment, should be ruled out. If the pain and tenderness are located in the belly of the BR muscle, which is essential for the diagnosis of BR muscle contraction, RTS is excluded. The RTS shows tingling and numbness rather than pain or tenderness at 3–4 cm distal from the lateral epicondyle. If the pain and tenderness is located on the origin of the BR muscle at the distal humerus proximal to the lateral epicondyle, it should be differentiated from pain and tenderness from the lateral epicondyle, determined by thorough physical examination. If the pain is located on the lateral wrist and fingers near the insertion of the BR muscle, the styloid process, it should be differentiated from de Quervain’s disease, CTS, trigger thumb, writer’s cramp, or cervical radiculopathy. If BR muscle spasm presents, combined subacromial bursitis should be checked and treated with subacromial bursa injection (Fig. 5).
BR muscle contraction commonly exists in patients with subacromial bursitis or lateral epicondylitis. Long-term persistent BR muscle pain may need both ultrasound-guided myofascial steroid injection and botulinum intramuscular injection.
BR muscle contraction is commonly found in the clinical field, sometimes combined with shoulder disorders, and is differentiated from other common forearm disorders according to the location of the tenderness or pain.
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