Physical therapy management of isolated anterior muscle paralysis.

This case report describes an uncommon musculoskeletal problem - isolated serratus anterior muscle paralysis - which may be secondary to nerve entrapment or neuralgic amyotrophy. The report illustrates (1) that a patient may describe generalized upper-extremity weakness that is actually due to weakness of a single muscle, (2) that the approach to intervention should be based on the pathophysiology of denervation and on the protracted healing process, and (3) that the exercise program and progression also should be based on the pathokinesiology associated with isolated serratus anterior muscle weakness. The principles outlined in this case report serve as a framework that may be useful in the physical therapy management of other peripheral neuropathies in which the prognosis for recovery is relatively good.

Isolated Paralysis of the

Serratus Anterior Muscle

Etiology

Two main causes have been proposed for isolated paralysis of the serratus anterior muscle. Some authors[1-5] attribute this phenomenon to an entrapment neuropathy involving the long thoracic nerve. Others[6-11] include it in the general condition known as neuralgic amyotrophy.

Entrapment neuropathies are lesions of individual peripheral nerves resulting from direct compression, stretch, angulation, or vascular compromise.[4] Some nerves, such as the long thoracic nerve, are particularly vulnerable to entrapment because of their anatomical locations. The long thoracic nerve is a motor nerve that typically arises from the cervical nerve roots of C-5, C-6, and C-7. Horwitz and Tocantins[1] dissected 100 shoulders in 50 human cadavers to study the nerve. They described the typical anatomic arrangement in which the fifth and sixth branches pierce through the scalenus medius muscle. These two branches unite shortly after exiting the scalenus medius muscle and join with the seventh and eighth branches (if present), which travel between the scalenus medius and scalenus anterior muscles. As the completed nerve pursues a vertical downward course, it passes 1.5 to 2.0 cm dorsal to the clavicle and is angulated over the second rib before descending the thoracic wall. The only muscle it supplies is the serratus anterior muscle.

One of the anatomical features of the nerve that predisposes it to injury is that it is tethered proximally to the scalenus medius muscle and has a distal connection to the serratus anterior muscle. Because of these attachments, and its passage over the second rib, the long thoracic nerve may be stretched, with shoulder depression or lateral flexion of the cervical spine to the opposite side.[1,2,12] Both forceful trauma involving shoulder depression[1-3,13] and repeated muscular stress[1,3,4,12,14] have been suggested as probable causes of entrapment injury to the nerve.

Most entrapment syndromes involving destructive lesions from mechanical friction or compression are thought to be preceded by symptoms of nerve irritation, including spontaneous pain, abnormal sensations, or muscle twitching.[5,15] Using the classification of nerve injury described by Sunderland,[16] entrapment of the long thoracic nerve would most likely be described as a second-degree injury, or axonotmesis. The pathology of a second-degree nerve injury includes axonal damage involving Wallerian degeneration, but the endoneurial sheath remains intact.[16] Complete functional recovery is expected in 3 to 12 months.[5]

Inflamed bursae in the proximity of the long thoracic nerve have also been implicated in entrapment, either by exerting direct mechanical pressure on the nerve or by contiguous inflammation.[1,2] The nocturnal pain reported by patients when assuming the supine position has been attributed to the mechanical insult applied to the nerve in this recumbent position.[2]

Advocates of the entrapment theory describe the patient's common complaints as dull aching pain centered about the shoulder, but also extending up the neck and down the arm[5]; shoulder pain or discomfort occurring during athletic activity, either on an acute, one-time basis or during repetitive vigorous activity[12]; and pain along the medial aspect of the scapula and lateral aspect of arm and forearm.[4]

The second possible cause of isolated serratus anterior muscle paralysis is neuralgic amyotrophy. Neuralgic amyotrophy is an uncommon neuromuscular syndrome of weakness and atrophy of muscles around the shoulder girdle and upper extremity, typically preceded by intense pain. Other terms used synonymously to describe this syndrome include "Parsonage-Turner syndrome," "acute brachial plexitis," "paralytic brachial neuritis," "shoulder-girdle neuritis," and "brachial plexus neuropathy."[7] Because an exact anatomical location for the lesion has not been clearly identified, the term "neuralgic amyotrophy" is preferred, as it does not confine the nerve involvement to the brachial plexus.[7,8]

No definite etiology has been established for neuralgic amyotrophy. Several precipitating factors are associated with the onset of symptoms. These factors include some form of unaccustomed strenuous exercise, recent surgery, a recent vaccination or foreign serum injection, or an antecedent infection. The infection may be viral, bacterial, or parasitic.[7]

In a study of 21 cases of neuralgic amyotrophy, Devathasan and Tong[8] used the following as their criteria for diagnosis: pain, atrophy and paralysis of shoulder girdle muscles, no report of a traumatic lesion or compression, full or partial recovery, and electromyographic (EMG) results revealing denervation or reduced numbers of functioning motor units of the involved muscles.

The patients described with neuralgic amyotrophy range in age from 3 months to 84 years.[8] Men are affected more than women.[11] There is no clear prevalence of one side over the other,[10] but in the case of isolated serratus anterior muscle paralysis, the right upper extremity is predominantly affected.[3,14] In one third of the patients, both upper extremities are involved. Typically, one upper extremity is more dramatically involved than the other, which may have subclinical findings.[9]

Neuralgic amyotrophy usually appears as pain during the convalescent stage of an illness or surgery.[7] The pain is occasionally transient, but usually lasts several weeks and in some cases even longer.[7] Typically, the patient complains of a sudden, severe onset in one or both shoulders. The pain is usually described as "sharp," "stabbing," "throbbing," or "aching."[9] Many patients are awakened at night with the onset of symptoms.[7] The discomfort is commonly worse at night and disturbs or prevents sleep. It may be intense enough to require strong analgesia.[17]

Location of the pain was detailed by Ferrini et al[10] in their observation of 58 cases over the course of 12 years. The regional distribution and percentage of incidence of pain was scapular (74%), side of neck (45%), shoulder (48%), axilla (15%), arm (76%), forearm (22%), and hand (36%).[10] Weakness is usually apparent once the pain subsides.

The likely muscle involvement, in order of decreasing frequency, is as follows: deltoid, supraspinatus, infraspinatus, serratus anterior, biceps brachii, triceps brachii, and wrist and finger extensors.[7] Sensory loss may occur, but is not as prevalent as motor loss and does not necessarily follow the same distribution as the motor loss.

The differential diagnosis includes a number of other pathological conditions such as poliomyelitis, motor neuron disease, cervical disk disease, cervical spondylosis, muscular dystrophy, diabetic amyotrophy, entrapment neuropathy, and primary shoulder disorders (such as rotator cuff tears, impingement syndromes, or calcifying tendinitis).[14,17,18]

The prognosis for patients who have neuralgic amyotrophy is good. Tsairis et al[9] described the outcome of 84 patients with neuralgic amyotrophy and reported functional recovery in 80% at 2 years and in 90% at 3 years. The measurement of functional recovery in this study was not clearly described, but seemed to be based on the patient's self-report.

Pathokinesiology of Isolated

Serratus Anterior Muscle

Paralysis

One action of the serratus anterior muscle is to hold the medial border of the scapula firmly against the thorax.[19] When the serratus anterior muscle is paralyzed, the inferior angle of the scapula becomes more prominent (Fig. 1), because there is virtually no other muscle to hold it against the thorax.(20) The other actions of the serratus anterior muscle are scapular upward rotation and abduction, which it can perform coupled with the forces of the upper and lower trapezius muscles, as the arm is elevated overhead (Fig. 2). Without concurrent upward rotation and abduction of the scapula, full humeral elevation cannot be achieved (Fig. 3).

The serratus anterior and trapezius muscles are also important in lending proximal stability to the shoulder girdle. They are synergists for the deltoid muscle acting at the glenohumeral joint.[21] If the deltoid muscle acts on the scapula with the humerus fixed, it produces downward scapular rotation.[21] Without the serratus anterior muscle functioning as a scapular stabilizer, both the humerus and the scapula move toward one another as the deltoid muscle contracts. As a result, the deltoid muscle becomes actively insufficient, or too short to develop adequate tension (Fig. 4).

Clinical Implications of Long

Thoracic Neuropathy and the

Subsequent Shoulder

Pathokinesiology

In this article, we have differentiated three stages associated with isolated long thoracic nerve injuries: acute, intermediate, and late. In the acute stage, denervation causes pain and changes in muscle physiology that result in fibrosis and eventually contracture.[16] The goals of treatment are to reduce pain, to prevent contracture, and to educate the patient regarding activity modification and upper-extremity Protection. Range of motion (ROM) can be used to prevent contracture of denervated muscles and the joints they surround. Protection of the shoulder joint is essential, beginning in the acute stage. With isolated serratus anterior muscle weakness, the scapula (and the glenoid fossa it houses) no longer upwardly rotates to accommodate the humeral head during overhead use of the upper extremity. The humeral head may impinge on the acromial process if the arm is used overhead without the normal scapulohumeral rhythm. The patient must be aware of the potential for injury and is advised to avoid overhead use of the extremity until the normal mechanics can be achieved. The patient should also avoid heavy lifting due to the lack of proximal stability at the shoulder. If nerve entrapment is suspected, the patient should eliminate causative occupational factors as well.[5]

The intermediate stage begins when the pain subsides. During this stage, the nerve is in the process of healing, but significant weakness exists. The denervated muscle still is at risk for contracture, as are the antagonist muscles. The goal of treatment is to maintain full ROM. Clinically, it has been established that stretching paralyzed muscles delays and may even prevent functional recovery once the involved muscles are reinnervated; therefore, stretching of the denervated muscle should be avoided.[16] If a muscle functions unopposed, in time it will adjust to its new position by becoming structurally shortened. Hence, coupled with the risk of contracture of the denervated muscle is the potential for shortening of the antagonist.[16] The antagonists to upward rotation of the scapula are the rhomboid, levator scapulae, and pectoralis minor muscles.[19,22] Passive stretching of these muscles is used to retain muscle length. Strengthening of the serratus anterior muscle begins only when reinnervation occurs.

The late stage is highlighted by progressive strength return and recovery of function. As the serratus anterior muscle becomes stronger and the shoulder girdle mechanics improve, the goals are to improve strength and to increase overhead use of the upper extremity. The long-term goal of treatment is to resume full functional use of the upper extremity. The upper and lower trapezius muscles, which primarily upwardly rotate the scapula, can and should be strengthened without overstretching the serratus anterior muscle. Careful analysis of the specific pathokinesiology must be utilized in designing an individualized ROM and strengthening exercise program. The clinician must always ensure that the serratus anterior muscle is strong enough to rotate the scapula throughout the ROM of the prescribed exercise, whether gravity eliminated or against gravity.

The typical prognosis for a patient with isolated serratus anterior muscle paralysis is full functional recovery in 3 months to 2 years. Fortunately, muscle tissue may survive denervation for at least 2 years.[16] Because the recovery period is sometimes protracted in these patients, physical therapy visits may be infrequent during the acute and intermediate states and increase frequency as significant muscle function returns during the late stage.

Case History

The patient was a 35-year-old right-hand-dominant male who developed pain that he described as "deep inside" and located at the dorsal aspect of the right arm. He recounted experiencing some discomfort for about 2 weeks, which suddenly became "extremely painful and unbearable" one night. He explained that the pain felt "like a bad charley horse" and noted that it seemed to be worse when he was lying supine. He attributed the pain to the hourly lifting requirements of approximately 9 to 14 kg (20-30 lb) associated with his part-time job in a bakery and having started an upper-extremity weight-lifting program 2 to 3 weeks prior to the onset of the pain. He stated that when his symptoms did not improve following 1 week of self-treatment of using over-the-counter anti-inflammatory medication, he went to see a general practitioner. The primary care physician ordered a roentgenogram, which did not indicate relevant pathology, and prescribed Relafen[R](*) (1 g per day).

The patient stated that despite taking his medication as prescribed, his pain continued to escalate to the point that he could not sleep. Four days after his visit to the physician, he went to the emergency department, where he received an intramuscular injection of 60 mg of Toradol[R],[dagger] a nonsteroidal anti-inflammatory agent, for pain control. He stated that he then finished his 10-day course of Relafen[R], with a gradual decrease in his pain and complete resolution approximately 6 weeks after the onset of pain. He noticed arm weakness when the pain subsided. Five months after the onset of shoulder pain, he returned to the general practitioner complaining of the persistent inability to use his right arm overhead. The physician referred the patient to physical therapy.

Physical Therapy Evaluation

On his initial visit the physical therapy, the patient's chief complaint was difficulty in using his arm overhead. He gave the specific examples of inability to lift his child onto his shoulders, inability to use his right upper extremity for lifting even light weights over shoulder height, and restricted ability to reach objects over shoulder height. He also noted "a funny feeling with lifting like my shoulder joint is sliding out of place," but denied having any shoulder pain at this point in time. The patient's past medical history was noncontributory.

The patient stated that he had returned to full-time employment. He was no longer working in a bakery, but was working as a medical biochemist, which did not require any lifting or overhead use of his upper extremities. He said that he had not participated in any regular exercise since the onset of his arm pain.

Measures

Manual muscle testing (MMT) was performed using the system described by Daniels and Worthingham.[23] The reliability of MMT grades has not been well established.[24] Manual muscle testing, however, is an integral part of the physical examination and provides information that is useful in the diagnosis, prognosis, and treatment of neuromuscular disorders.[19] Active range of motion (AROM) and passive range of motion (PROM) were measured using a universal goniometer. Goniometric measurements of shoulder PROM have high intratester reliability.[25] Boone and colleagues[26] concluded that the intratester reliability of goniometric measurements of upper-extremity AROM is higher than intertester reliability. As a result, they suggest that when more than one tester measures the same upper-extremity motion, changes in ROM should exceed 5 degrees in order to demonstrate improvement.[26] Intertester reliability s relevant, as this case report describes a patient who relocated to another state during the course of his treatment. His first 5 months of physical therapy measurement and treatment was done by one therapist, and the last 3 months was done by a second therapist.

Visual observation was used for assessment of general muscle symmetry and to assess the movement of this patient's scapula specifically. Goniometric measures were not used because it is difficult to reproduce the reference point on which to measure scapular motion.[27] This patient's active shoulder flexion and abduction were also videotaped during his second and seventh visits to physical therapy. Videotaping made it possible to slow down the motion for more accurate visualization of the shoulder biomechanics and to record the subtle changes in scapular AROM on film.

Findings

The patient was a well-developed white male who did not report having acute pain. The patient had no observable muscle atrophy throughout the shoulder girdle, but he did exhibit hypertrophy of the right upper trapezius and rhomboid muscles (Fig. 5).

Using MMT, the right serratus anterior muscle strength was Zero; no palpable muscle contraction was present. The patient appeared to have Normal strength bilaterally in his upper extremities distal to and including the elbow region. Proximally, he had Normal strength on the left side, but weakness of the shoulder flexors and abductors on the right side (Tab. 1). With the arm held at his side, however, these muscles appeared to be normal. The patient had full AROM of the left shoulder complex, but decreased right scapulothoracic and glenohumeral AROM (Tab. 2) with pronounced scapular winging during abduction and flexion of the humerus (Figs. 3 and 4). He had full PROM of the shoulders bilaterally in all directions, with a tissue stretch end-feel.

Table 1. Initial Evaluation Findings
for Proximal Upper-Limb Strength(a)

Joint Movement          Left     Right

Shoulder
 Flexion                Normal   Fair minus
 Extension              Good     Good
 Abduction              Normal   Fair minus
 Horizontal abduction   Normal   Normal
 Medial rotation        Normal   Normal
 Lateral rotation       Normal   Normal

Scapular
 Elevation              Normal   Normal
 Adduction              Good     Good
 Depression and
   adduction            Good     Good
 Adduction and
   downward
   rotation,            Normal   Normal
 Abduction and
   upward rotation      Normal   Zero

"Manual muscle testing was performed using
the system described by Daniels and
Worthingham.[23]

Table 2. Initial Evaluation Findings
for Shoulder Active Range of Motion (in
Degrees)

Direction          Left   Right

Flexion             165    95(a)
Abduction           180   110(a)
Extension            50    50
Medial rotation      50    35
Lateral rotation     80    95

(a) Scapular winging present.

The patient had no complaints of pain with cervical AROM or PROM or with resistive testing of the neck musculature. He exhibited 2+ bilateral biceps brachii, brachioradialis, and triceps brachii muscle reflexes. His sense of light touch and sharp versus dull stimulation was intact throughout both upper extremities.

Interpretation

Weakness in shoulder flexion and abduction was interpreted as secondary to absent serratus anterior muscle function and the associated lack of scapular active mobility and stability. Because the serratus anterior muscle is the only muscle innervated by the long thoracic nerve, isolated pathology involving this nerve was thought probable. Further testing was indicated prior to initiating physical therapy. The referring physician was contacted and made aware of these physical therapy findings; he then referred the patient to an orthopedic surgeon. Following his clinical examination of the patient, the orthopedic surgeon concurred with the physical therapy assessment of isolated serratus anterior muscle weakness and ordered EMG testing.

Six months after the initial onset of right arm pain, the patient underwent nerve conduction and EMG analysis of the right shoulder complex. The right serratus anterior muscle EMG showed normal insertional activity and no spontaneous activity. There were mild to moderately increased numbers of long-duration, complex motor unit potentials and a normal recruitment and interference pattern. The results demonstrated evidence of a chronic, inactive, right long thoracic nerve injury. The serratus anterior muscle was reinnervating, according to the neurologist interpreting the EMG findings. Additionally, there was no evidence of brachial plexopathy, cervical radiculopathy, or polyneuropathy.

The etiology of the long thoracic neuropathy was not clear in this patient. Arguments could probably be made to categorize the patient presented as having either neuralgic amyotrophy or long thoracic nerve entrapment. The two conditions seem to overlap in cases in which the onset of symptoms occurs following strenuous exercise. Perhaps because of the anatomical configuration of the long thoracic nerve, the traction to the shoulder girdle and repeated muscular stress associated with lifting caused nerve compression. The patient, however, fulfills the criteria for the diagnosis of neuralgic amyotrophy, depending on the definition used to describe a compressive or traumatic lesion.[8] Unaccustomed strenuous exercise without direct trauma has been included as a precipitating event in neuralgic amyotrophy.[7,9] Stewart[28] states that patients who have no history of major trauma and who experience a lot of shoulder pain most likely have neuralgic amyotrophy.

Regardless of the cause, this patient did exhibit a long thoracic neuropathy and a good prognosis for recovery. By the time the patient was referred to physical therapy, he was past the acute stage, so pain was not a problem. He was judged to be in the intermediate stage, and his goals were set accordingly.

Physical Therapy Goals

Because this patient was in the intermediate stage of recovery upon initial evaluation, the immediate goals were to prevent loss of ROM at the shoulder, for the patient to demonstrate an understanding of activity modification and upper-limb protection, and to strengthen the lower trapezius muscle for protection of the serratus anterior muscle from overstretching. As the serratus anterior muscle becomes reinnervated (late stage), the modified goals are to increase strength of the serratus anterior muscle to normalize scapulohumeral rhythm and to improve overhead use of the upper extremity within the available scapulohumeral ROM. The long-term functional goals for this patient included the ability to lift his child onto his shoulders, to lift weighted objects overhead, and to use the arm for overhead reaching.

Treatment

Because this patient was in the intermediate stage of recovery, his treatment consisted of a home exercise program with follow-up visits at regular intervals. Education was essential. He was instructed in the importance of activity modification to protect the denervated muscle and to prevent rotator cuff impingement. He was also taught the stretching exercises described below, to be performed daily (five repetitions each with a 20-second hold). Because these exercises were passive, the patient was instructed to teach his wife to assist him. To maintain full medial (internal) and lateral (external) rotation it the glenohumeral joint, he was instructed to lie supine with the shoulder in 90 degrees of abduction. With the arm supported and the elbow flexed to 90 degrees, the humerus was rotated laterally and medially to the extremes of available motion.

Next, while the patient was lying on his side, with the scapula passively upwardly rotated, the upper extremity was moved through the full pain-free range of flexion. In a prone position, with the scapula passively upwardly rotated, the upper extremity was moved through the full pain-free range of abduction. Finally, passive shoulder retraction was carried out in a supine position to stretch the pectoralis minor muscle.

Moist heat and massage were not indicated because the patient was pain-free at the time he was referred to physical therapy. Electrical stimulation was not utilized because there seems to be no conclusive evidence that it influences recovery.

Strengthening exercises for the lower trapezius muscle, the serratus anterior muscle, and the rotator cuff were to be performed every other day (30 repetitions each). Strengthening of the lower trapezius muscle has been described as one of the major aims of therapy in the case of serratus anterior muscle paralysis secondary to the ability of the lower trapezius muscle to protect the serratus anterior muscle from elongation.[3] The patient performed the lower trapezius muscle exercise in the prone-lying position, with the affected upper extremity over the side of the table (Fig. 6). In this position, the patient was instructed to laterally rotate the shoulder and then flex through the full pain-free ROM. The prone position was selected to reduce the effects of gravity and to allow scapular mobility, which would be hindered in the supine position. Although contraction of the lower trapezius muscle does produce some scapular adduction, this is not its primary action. This patient was initially thought to have hypertrophy of the upper trapezius muscle, probably secondary to increased functional demands placed on the muscle; strengthening exercises were therefore not specifically addressed.

The patient was also instructed in therapeutic exercise for serratus anterior muscle strengthening. The first exercise requires use of the serratus anterior muscle as a scapular abductor (Fig. 7). Lying supine, the patient was directed to hold the shoulder in the scapular plane (30[degrees] anterior to the frontal plane) and to project the upper extremity anterolaterally, away from the table. The scapular plane was chosen to minimize the action of the pectoralis muscles. As the patient's strength improved, the exercise was performed against low-resistance elastic.

The second exercise is based on the procedure of Johnson and Kendall,[3] who described their experience with 20 cases of isolated serratus anterior muscle paralysis. The exercise involves attempting to contract the serratus anterior muscle, in its function as a scapular rotator, when the muscle is significantly weak (Fig. 8). The patient is positioned supine, with the affected arm resting overhead on pillows, and is instructed to press the arm down on the pillows in the direction of shoulder flexion. The patient is directed to bring the inferior angle of the scapula forward during this movement and may be encouraged to palpate the serratus anterior muscle with the opposite hand during the exercise.[3]

Because the patient was advised to decrease the overhead use of the extremity and not to perform any heavy lifting, he may have been susceptible to mild disuse atrophy of the proximal musculature. General strengthening exercises for the medial and lateral rotators of the humerus were therefore included. The patient was instructed to perform resisted shoulder medial and lateral rotation using elastic, while maintaining his arm at his side to provide proximal upper-limb stability.

The patient was followed for 5 months, and he then moved out of state. During that 5-month period, his physical therapy appointments were scheduled approximately every 3 weeks to ensure that he maintained shoulder ROM and demonstrated an understanding of his exercises and to determine the necessity for exercise progressions based on strength return in the serratus anterior muscle.

Outcome

After 5 months of physical therapy, and 10 months after the onset of right shoulder pain, the patient had retained full shoulder PROM. The patient's serratus anterior muscle strength improved to Poor plus, but his muscle strength was otherwise unchanged throughout the upper extremity. The increase in serratus anterior muscle strength resulted in increased scapular abduction and upward rotation during humeral elevation. As a result, he had increased shoulder AROM to 145 degrees of abduction and 155 degrees of flexion. He demonstrated an understanding of activity modification and limb protection. At that time, the patient moved out of state; he was advised to continue physical therapy in his new location.

The patient reported that after moving he followed up with physical therapy, but was limited to only three monthly visits secondary to restrictions from his health maintenance organization. He reported that his shoulder started to dramatically improve approximately 1 year after the onset of pain. The patient's medical records were obtained from the treating physical therapist. At the time of the patient's last visit, 13 months after the onset of pain, his serratus anterior muscle strength had increased to Good plus. He had scapular winging, but full right shoulder AROM.

At the writing of this case report, it had been approximately 17 months since the onset of pain and the patient stated that he felt "90% improvement" in the use of his right shoulder. He reported pain-free use of his affected upper extremity, but noticed that the right upper extremity fatigued more easily than the left upper extremity. He stated that he was able to lift light weights, including his child, over his head and no longer had the sensation of the shoulder sliding out of place.

Summary

The physical therapy management of a patient with isolated paralysis of the serratus anterior muscle was described. Emphasis was placed on the pathophysiology and pathokinesiology and the direct implications for the selection of therapeutic exercises. The specific ROM and strengthening exercises utilized were outlined.

The patient was referred to physical therapy for strengthening exercises 22 weeks after the onset of his shoulder pain. At the time of his physical therapy evaluation, he was pain-free but had virtually no palpable activity in the serratus anterior muscle. Electromyography confirmed an isolated long thoracic nerve injury. He was advised to modify his use of the involved upper extremity and instructed in a home exercise program. He was followed approximately every 3 weeks for 5 months before moving to another state. over the course of his treatment, the patient was able to maintain full PROM at the left shoulder and his serratus anterior muscle strength improved to Poor plus. In a follow-up conversation with the patient 17 months after the onset of shoulder pain, he reported that he attended physical therapy in his new place of residence and had experienced a 90% improvement in his ability to use the right shoulder.

Acknowledgments

We thank Emy Villanueva, PT, for her assistance in analyzing the pathokinesiology of this patient's shoulder and for critical reading of the manuscript. We especially thank the patient discussed in this case report for his willingness to allow the presentation of his shoulder diagnosis and treatment.

References

[1] Horwitz MT, Tocantins LM. An anatomical study of the role of the long thoracic nerve and the related scapular bursae in the pathogenesis of local paralysis of the serratus anterior muscle. Anat Rec. 1938;71:375-385. [2] Horwitz MT, Tocantins LM. Isolated paralysis of the serratus anterior (magnus) muscle. J Bone Joint Surg. 1938;20:720-725. [3] Johnson JTH, Kendall HO. Isolated paralysis of the serratus anterior muscle. J Bone Joint Surg [Am]. 1955;37:567-574. [4] Fisher MA, Gorelick PB. Entrapment neuropathies: differential diagnosis and management. Postgrad Med. 1985;77:161-174. [5] Sunderland S. Nerves and Nerve Injuries. 2nd ed. Edinburgh, Scotland: Churchill Livingstone; 1978. [6] Parsonage MJ, Turner JWA. Neuralgic amyotrophy: the shoulder girdle syndrome. Lancet. 1948;i:973-978. [7] Aymond JK, Goldner JL, Hardaker WT. Neuralgic amyotrophy. Orthop Rev. 1989;18:1275-1279. [8] Devathasan G, Tong HI. Neuralgic amyotrophy: criteria for diagnosis and a clinical with electromyographic study of 21 cases. Aust AZJ Med. 1980;10:188-191. [9] Tsairis P, Dyck PJ, Mulder DW. Natural history of brachial plexus neuropathy. Arch Neurol. 1972;27:109-117. [10] Ferrini L, Della-Torre P, Perticoni G, Cantisani TA. Neuralgic amyotrophy of the shoulder girdle. Ital J Orthop Traumatol 1986;12:223-231. [11] Turner JWA, Parsonage MJ. Neuralgic amyotrophy (paralytic brachial neuritis), with special reference to prognosis. Lancet. 1957;ii:209-212. [12] Gregg JR, Labosky D, Harty M, et al. Serratus anterior paralysis in the young athlete. J Bone Joint Surg [Am]. 1979;61:825-831. [13] Goodman CE, Kenrick MM, Blum MV. Long thoracic nerve palsy: a follow-up study. Arch Phys Med Rehabil. 1975;56:352-355. [14] Foo CL, Swann M. Isolated paralysis of the serratus anterior. J Bone Joint Surg [Br]. 1983;65:552-556. [15] Pratt NTE. Neurovascular entrapment in the regions of the shoulder and posterior triangle of the neck. Phys Ther. 1986;66:1894-1900. [16] Sunderland S. Nerve Injuries and Their Repair: A Critical Appraisal. Edinburgh, Scotland: Churchill Livingstone; 1991. [17] Neuralgic amyotrophy: still a clinical syndrome. Lancet. 1980;ii:555-556. Editorial. [18] Favero KJ, Hawkins RH, Jones MW. Neuralgic amyotrophy. J Bone Joint Surg [Br]. 1987;69:195-198. [19] Kendall FP, McCreary EK. Muscles: Testing and Function. 3rd ed. Baltimore, Md: Williams and Wilkins; 1983. [20] Soderberg GL. Kinesiology.. Application to Pathological Motion. Baltimore, Md: Williams & Wilkins; 1986. [21] Norkin CC, Levangie PK. Joint Structure and Function: A Comprehensive Analysis. Philadelphia, Pa: FA Davis Co; 1983. [22] Schenkman M, Rugo De Cartaya V. Kinesiology of the shoulder complex. J Orthop Sports Phys Ther. 1987;8:438-450. [23] Daniels L, Worthingham C. Muscle Testing: Techniques of Manual Examination. Philadelphia, Pa: WB Saunders Co; 1980. [24] Lamb RL. Manual muscle testing. In: Rothstein JM, ed. Measurement in Physical Therapy. New York, NY: Churchill Livingstone Inc; 1985:47-55. [25] Riddle DL, Rothstein JM, Lamb RL. Goniometric reliability in a clinical setting: shoulder measurements. Phys Ther. 1987;67:668-673. [26] Boone DC, Azen SP, Chun-Mei L, et al. Reliability of goniometric measurements. Phys Ther. 1978;58:1355-1360. [27] Paine RM, Voight M. The role of the scapula. J Orthop Sports Phys Ther. 1993; 18:386-391. [28] Stewart JD. Focal Peripheral Neuropathies. New York, NY: Raven Press; 1983:140-156.