Background and Purpose. The authors found no literature describing adhesive capsulitis as a consequence of spinal accessory nerve injury and no exercise program or protocol for patients with spinal accessory nerve injury. The purpose of this case report is to describe the management of a patient with adhesive capsulitis and spinal accessory nerve injury following a carotid endarterectomy. Case Description. The patient was a 67-year-old woman referred for physical therapy following manipulation of the left shoulder and a diagnosis of adhesive capsulitis by her orthopedist. Spinal accessory nerve injury was identified during the initial physical therapy examination, and a program of neuromuscular electrical stimulation was initiated. Outcomes. The patient had almost full restoration of the involved muscle function after 5 months of physical therapy. Discussion. This case report illustrates the importance of accurate diagnosis and suggests physical therapy intervention to manage adhesive capsulitis as a consequence of spinal accessory nerve injury.

Spinal accessory nerve injury is documented in the literature as a complication of various surgical procedures or trauma. Surgical procedures contributing to iatrogenic spinal accessory nerve injury are carotid endarterectomy, biopsy of the cervical lymph nodes,1 radical neck dissection for the treatment of neck and head tumors,2 and surgical procedures in the posterior triangle.3

The spinal accessory nerve arises superficially from a series of filaments located behind the root filaments of the vagus nerve and from the lateral surface of the medulla and upper cervical spinal cord and leaves the cranial cavity through the jugular foramen.4 The spinal accessory nerve leaves the jugular foramen and passes laterally and backward, either posterior or anterior to the internal jugular vein, then descends obliquely to the upper part of the sternocleidomastoid muscle.5 At this location, the spinal accessory nerve is vulnerable to injury during surgical procedures. It pierces the deep surface of the sternocleidomastoid muscle, giving off branches for its innervation. It then runs along the deep surface of the sternocleidomastoid muscle to emerge at its posterior border just above the midpoint of the length of the muscle. The nerve then crosses the posterior triangle of the neck on the anterior surface of the levator scapulae and rhomboid muscles. In this region, the nerve is covered only by subcutaneous fat and skin. From the posterior part of the posterior triangle, the nerve descends on the anterior surface of the trapezius muscle, giving off branches to the trapezius muscle6 (Fig. 1).

Figure 1.

Anatomy of the posterior triangle.

In addition to spinal motor distribution to the sternocleidomastoid and trapezius muscles, the spinal accessory nerve provides laryngeal and cranial innervation. Therefore, compression in the jugular foramen can affect the spinal accessory nerve, causing dysphagia, hoarseness, and dysarthria. This combination of clinical findings may indicate involvement of cranial nerves IX, X, and XI (the so-called jugular foramen syndrome or Jackson syndrome), whereas involvement of the spinal accessory nerve proximal to the sternocleidomastoid muscle would affect the sternocleidomastoid and trapezius muscles.4 Distal compression (as in the posterior triangle) would involve the trapezius musculature alone.4

Nakamichi and Tachibana1 provided only general exercise recommendations for treatment of spinal accessory nerve injury. We believe that spinal accessory nerve injury may lead to decreased mobility in the involved shoulder and may contribute to adhesive capsulitis. The purpose of this case report is to demonstrate specific physical therapy interventions, including proximal scapular stabilization exercise, proprioceptive neuromuscular facilitation (PNF), neuromuscular electrical stimulation (NMES), shoulder strengthening exercises with Thera-Band,* and pool exercises for a patient with spinal accessory nerve injury complicated by adhesive capsulitis.

Case Description

Patient History and Systems Review

The patient was a 67-year-old woman who was referred for physical therapy 2 weeks after left shoulder manipulation for adhesive capsulitis and 11 weeks after a left carotid endarterectomy. Her cardiologist referred her to an orthopedic surgeon approximately 1 month after the endarterectomy with complications of left proximal clavicular pain and limited range of motion of the left shoulder. The orthopedic surgeon diagnosed adhesive capsulitis.

The patient reported that her shoulder stiffness began 2 days after her neck surgery. Her past medical history also included a right carotid endarterectomy 2 months prior to the left endarterectomy, hypertension for which she was taking spironolactone (25 mg twice daily), a C2 fixation after a motor vehicle accident 8 years previously, and the resection of a right parotid tumor 13 years before. The patient had no previous injury to the left shoulder. She underwent radiography prior to the manipulation, which revealed a normal joint relationship of the left shoulder.

The patient was a retired orthopedic registered nurse who reported that she was unable to lift her left arm high enough to wash her left axilla until after the manipulation, when her shoulder abduction improved to 45 degrees. She said that she also had difficulty with overhead reaching, doing dishes, washing and styling her hair, dressing with the left upper extremity, and holding her 4-month-old grandchild. Her recreational activities were also affected because she was unable to complete her swimming routine due to left shoulder pain and limited motion. Her goals were to regain mobility of her left shoulder to return to her previous levels of activities of daily living, which included swimming, holding her infant grandchild, and hanging clothes on the line.

Examination: Tests and Measures

Pain and posture.

The patient reported constant anterior clavicular pain, which she rated 3 on a visual analog scale with 0 indicating no pain and 10 indicating the worst possible pain.7 She had a notable depression and forward translation of the left shoulder, with atrophy in the left anterior supraclavicular region and left trapezius muscle (Fig. 2). The left scapula was protracted, abducted, and rotated clockwise with increased distance of 9.0 cm from the inferior angle to the T8 spinous process as compared with 7.0 cm on the right. This was measured by the therapist (KH) 2 times for accuracy using a standard metric ruler.

Figure 2.

The patient demonstrated left shoulder depression due to observable trapezius muscle weakness at the start of treatment.

Joint integrity, mobility, and range of motion.

Initially, the patient had 120 degrees of active left shoulder flexion, and active abduction was limited to 60 degrees. The therapist (KH) collected all data using a goniometer. Riddle et al8 concluded that measurements of passive range of motion in flexion and abduction are most reliable when the same physical therapist takes the measurements with either a large or small goniometer. The measurements were repeated by 2 additional therapists, who found comparable results for range of motion in the shoulder joint. With lateral (external) rotation, the patient could fully reach behind her head with her hand, with compensation of left shoulder girdle elevation. She had full medial (internal) rotation in the hand-behind-back position and full passive range of motion of the glenohumeral joint with manual scapular stabilization of the examiner's left hand over the lateral inferior aspect of the left scapula. She reported anterior shoulder pain, which she rated as 4 on a scale of 0 to 10 at the end-range of active and passive movements in all directions. Cervical active range of motion was symmetrically limited to 25 degrees of lateral flexion and 35 degrees of cervical rotation due to left-sided weakness and right-sided muscle tightness. She had no limitation of cervical flexion and extension, and she did not report pain with cervical motion testing.

Muscle performance.

Strength testing9 of the left upper extremity revealed 1/5 strength of the left upper trapezius muscle, 2+/5 strength of the left middle trapezius muscle, 2−/5 strength of the left lower trapezius muscle, and 1/5 strength of the left sternocleidomastoid muscle, with minimal contraction noted. The patient had 2+/5 strength of the middle and anterior deltoid muscles and 5/5 strength throughout the rest of her left shoulder and both elbows, wrists, and hands. Right lower trapezius muscle strength was 3+/5, middle trapezius muscle strength was 4/5, and upper trapezius and sternocleidomastoid muscle strength was 5/5. Further testing showed that the left upper and lower trapezius muscles could be stimulated to contraction with NMES with the electrodes placed over the motor points.10

To assess the reliability of the measurements, 3 physical therapists with 5, 13, and 25 years of experience repeated the manual muscle testing and measurements of range of motion. They reported data for range of motion within 5 degrees and consistent scores for manual muscle testing.

Cranial nerve integrity.

The patient had no dysphagia, dysarthria, or hoarseness, indicating that the spinal accessory nerve was not affected in the jugular foramen.


Evaluation of the examination findings indicated spinal accessory nerve involvement, because the spinal accessory nerve provides motor innervation to the trapezius and sternocleidomastoid muscles, which were weak on the left side. The patient's history and examination findings prompted the physical therapist (KH) to try to identify the most probable causes of this clinical picture. Sweeney and Wilbourn11 described multiple cases of spinal accessory nerve palsy following carotid endarterectomy. In case reports of a similar nature,1,12 the authors reported recovery of function in an average of 6 to 12 months. Based on prior cases and the fact that the left trapezius and sternocleidomastoid muscle contraction occurred with NMES and manual muscle testing, we believed that the patient's postsurgical complications would improve to premorbid levels within this time frame. The plan to restore function included the use of NMES to improve muscle performance, range of motion exercises to reduce restrictions, and clinical and home exercise programs to improve physical tasks and activity levels. The referring orthopedic physician was contacted regarding the physical therapy examination, and he agreed to the recommended course of treatment. He stated that he would see the patient as scheduled, 4 weeks after the date of referral.


A physical therapy program was initiated 11 weeks after the left carotid endarterectomy. It included outpatient treatment sessions 2 times a week for 3 weeks (Tab. 1), followed by appointments at 16, 18, 22, and 30 weeks after surgery, for a total of 10 physical therapy sessions. The patient was provided with written and illustrated home exercise program instructions (Tabs. 2 and 3) and a chart to help her record daily exercise performance. Treatment goals were to maintain the range of motion obtained by manipulation and to strengthen the muscles affected by the spinal accessory nerve injury.

Table 1.

Clinical Intervention Programa

Table 2.

Home Exercise Program Beginning 11 Weeks After Carotid Endarterectomya

Table 3.

Stretching and Strengthening Home Exercises

During the first treatment session, the patient was given a shoulder sling to support and elevate the left shoulder girdle to improve symmetry and was instructed in its use. With the patient positioned supine, the physical therapist performed passive range of motion and manual mobilization of the left glenohumeral joint. Manual stabilization of the lateral inferior angle of the left scapula was provided by the therapist's right hand. With the patient in a right side-lying position, the left scapula was mobilized by the physical therapist into adduction. The physical therapist educated the patient in wand exercises into shoulder elevation, abduction, and lateral rotation. She did 3 sets of 10 repetitions and was asked to continue these exercises at home.

The patient was then positioned in right side lying, and NMES was used with biphasic pulses in burst mode applied via electrodes over the motor points10 of the left upper and lower trapezius muscles. Neuromuscular electrical stimulation13 was used to prevent trapezius muscle atrophy initially (sessions 1 and 2) and then to re-educate the scapular muscles in conjunction with scapular PNF exercises (sessions 3–6). A frequency of 50 pulses per second was used, with an “on time” of 10 seconds and an “off time” of 50 seconds,14 and the intensity was set for an observable muscle co-contraction. McConnell tape was applied over protective tape from the posterior-lateral left acromion diagonally across the back and ended just lateral to the thoracic spinous process T10.15 After passive range of motion and NMES in the first 2 sessions, McConnell taping and manual scapular stabilization were used with active range of motion to 90 degrees of shoulder elevation into abduction. At session 3, the patient began cervical PNF.16 For the treatment, the patient was positioned supine with her head off the table and shoulders even with the table's edge. The therapist passively guided the patient's head from cervical extension and right rotation into cervical flexion and left rotation. Treatment progressed in sessions 4, 5, and 6 by adding active range of motion during PNF and manually resisted isometric exercises of the sternocleidomastoid muscle.

In the next 5 sessions, the same regimen was followed, with progressions as described in Table 1. The home program progressed from passive support of a sling and passive range of motion exercises of the shoulder through active assistive to resistive exercises. A general strengthening program for the left upper quadrant17 emphasized improvement of proximal shoulder stability in a gravity eliminated to standing progression. The patient began a pool program of bilateral shoulder horizontal abduction and breaststroke simulation during ambulation after her first 6 sessions (4 weeks after initiation of physical therapy and 15 weeks following left endarterectomy). Her goal was to resume the pool exercises that she had done before her left carotid endarterectomy.


During the final session, 6 months after the onset of symptoms, the patient had nearly full strength, with a return of function of her left shoulder with improved glenohumeral and scapular position (Fig. 3). She was able to hold her infant grandchild, hang clothes on the line, dress without difficulty, wash and style her hair, and place objects into upper cabinets and on shelves with either arm. She documented her exercise program on a chart indicating exercises, repetitions, and time. Passive mobility remained unchanged, using full range of motion in the left glenohumeral joint. In standing, she had active left shoulder forward flexion to within 10 degrees of right shoulder forward flexion. Although abduction improved from 60 degrees to 150 degrees with active range of motion and fully with passive range of motion, weakness of the lower trapezius muscle appeared to limit her active range of motion of left shoulder abduction to 150 degrees. Thus, the final home program consisted of lower trapezius muscle strengthening exercise and continued scapular stabilization exercise (Tabs. 2 and 3). All cervical ranges of motion improved bilaterally (45° of rotation and 35° of lateral flexion). Left anterior deltoid muscle strength improved to 5/5, upper trapezius and middle deltoid muscle strength improved to 4+/5, left middle trapezius muscle strength improved to 4/5, and left lower trapezius muscle strength improved to 3−/5 (as compared with 3+/5 right lower trapezius muscle strength with manual muscle testing). The sternocleidomastoid muscle improved from 1/5 (Fig. 4) to 4+/5, with evidence of visible muscle contraction (Tab. 4, Fig. 5).

Figure 3.

Five months after initial session, the patient demonstrated improved left shoulder position with notable trapezius muscle recovery.

Figure 4.

At the start of treatment, left sternocleidomastoid muscle contraction was diminished with manual muscle testing.

Figure 5.

Five months after initial session, there was visible left sternocleidomastoid muscle contraction, indicating increased strength with manual muscle testing.

Table 4.

Initial and Final Active Range of Motion (AROM) and Manual Muscle Testing (MMT) Data

The distance between the spinous process of T8 and the left inferior angle decreased to 7 cm, as it was on the right side, although the left scapula was approximately 1 cm higher than the right scapula. Finally, the patient performed a lift test on a pulley system where she was asked to do 10 repetitions of shoulder shrugs with a maximum load established with the uninvolved extremity. This test was not conducted at the initial evaluation due to lack of sufficient muscle strength in the affected extremity. At the exit evaluation, the maximum lift on the right was 49.9 kg (110 lb) for 2 sets of 10 repetitions. The patient was able to lift 49.9 kg 7 times for the first set and 9 times for the second set on the involved extremity.


Our physical therapy program deviated from traditional treatment for adhesive capsulitis. After manipulation by the orthopedic surgeon, we concentrated more on proximal stability, muscle re-education, stimulation, and strengthening than on heat modalities and range of motion. The patient's posture, past medical history, and symptoms suggested a spinal accessory nerve injury. She responded to muscle stimulation distal to the nerve injury, and posture and function improved in less than 6 months, which suggests accessory nerve neurapraxia. The 2 other classifications of nerve injury are axonotmesis (interruption of the axon with subsequent Wallerian degeneration; connective tissue of the nerves remains intact) and neurotmesis (complete transection of the nerve).18

Studies12,19 have demonstrated full recovery from spinal accessory nerve palsy in about 1 year. Our patient showed marked improvement in quality of motion and posture in 5 months following the exercise program, which further suggests postsurgical neurapraxia. Without physical therapy, the patient probably would have recovered in 6 to 12 months, as suggested in the literature. The fact that our patient's limitations improved following upper trunk stabilization exercise (postexercise findings of proximal weakness due to a probable compression or stretch injury to the spinal accessory nerve following a left carotid endarterectomy) emphasizes the need for a complete evaluation. We believe that the complete evaluation, including not only the involved area but the entire upper quadrant, contributed to finding the source of the shoulder pain and limitation. If the adhesive capsulitis had been caused secondary to trauma, immobilization, or systemic disease, we would have changed the course of the treatment.20 This evaluation includes use of observation skills, complete cervical and thoracic assessment, integration of findings with medical history, and basic neurologic examination as outlined in the American Physical Therapy Association's Guide to Physical Therapist Practice.21 This case illustrates the responsibility of a physical therapist to perform a comprehensive orthopedic and neurologic examination of not only the involved structures but adjacent areas as well.


  • Both authors provided writing, data analysis, and project management. Mr Laska and Richard Lambie, PT, provided concept/project design. Ms Hannig provided data collection. The authors acknowledge the support and assistance of Mr Lambie, Mark Dutton, PT, Robert W Galbreath, PhD, and Maureen McKenna, PT, PhD, in the preparation of the manuscript.

    This project was approved by the Ohio Valley Medical Center Committee for the Protection of Human Subjects.

    This work was presented at the Combined Sections Meeting of the American Physical Therapy Association; February 14–18, 2001; San Antonio, Tex.

  • * The Hygenic Corp, 1245 Home Ave, Akron, OH 44310.

  • Received December 31, 1999.
  • Accepted September 4, 2000.


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