“Winged” Eagle’s syndrome: neurophysiological findings in a rare cause of spinal accessory nerve palsy. Illustrative cases

Eric C Mitchell Departments of Surgery,

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Kitty Y Wu Division of Plastic Surgery, Mayo Clinic, Rochester, Minnesota

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Fawaz Siddiqi Departments of Surgery,

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John Yoo Otolaryngology—Head and Neck Surgery

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Pavlo Ohorodnyk Medical Imaging, and

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Douglas Ross Departments of Surgery,

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Thomas A Miller Physical Medicine and Rehabilitation, Western University, London, Ontario, Canada; and

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BACKGROUND

Eagle’s syndrome (ES) classically describes dysphagia, globus sensation, and otalgia from an elongated and calcified styloid process or stylohyoid ligament. Compression of the spinal accessory nerve (SAN) has not been reported as an associated feature of ES or related variants.

OBSERVATIONS

The authors describe two cases of an atypical “winged” variant with SAN palsy resulting from compression by a posteriorly angulated or calcified styloid process. Both patients exhibited lateral scapular winging and atrophy of the trapezius and sternocleidomastoid muscles. Electrophysiological studies demonstrated motor unit preservation; therefore, surgical exploration, styloidectomy, and SAN decompression were performed through a transcervical approach. Postoperatively, both patients had improvements in pain and shoulder mobility, the return of muscle strength, and electrophysiological evidence of trapezius reinnervation.

LESSONS

Compression of the SAN, which can be identified both clinically and on electrodiagnostic testing, is an atypical finding that can result from a posteriorly angulated or calcified styloid process. This winged variant of ES should be included in the differential for SAN palsy, and a multidisciplinary approach is recommended for assessment and management.

ABBREVIATIONS

CMAP = compound muscle action potential; CT = computed tomography; DISH = diffuse idiopathic skeletal hyperostosis; EMG = electromyography; ES = Eagle’s syndrome; FSHD = facioscapulohumeral dystrophy; IJV = internal jugular vein; MRI = magnetic resonance imaging; NCS = nerve conduction study; SAN = spinal accessory nerve; TP = transverse process

BACKGROUND

Eagle’s syndrome (ES) classically describes dysphagia, globus sensation, and otalgia from an elongated and calcified styloid process or stylohyoid ligament. Compression of the spinal accessory nerve (SAN) has not been reported as an associated feature of ES or related variants.

OBSERVATIONS

The authors describe two cases of an atypical “winged” variant with SAN palsy resulting from compression by a posteriorly angulated or calcified styloid process. Both patients exhibited lateral scapular winging and atrophy of the trapezius and sternocleidomastoid muscles. Electrophysiological studies demonstrated motor unit preservation; therefore, surgical exploration, styloidectomy, and SAN decompression were performed through a transcervical approach. Postoperatively, both patients had improvements in pain and shoulder mobility, the return of muscle strength, and electrophysiological evidence of trapezius reinnervation.

LESSONS

Compression of the SAN, which can be identified both clinically and on electrodiagnostic testing, is an atypical finding that can result from a posteriorly angulated or calcified styloid process. This winged variant of ES should be included in the differential for SAN palsy, and a multidisciplinary approach is recommended for assessment and management.

ABBREVIATIONS

CMAP = compound muscle action potential; CT = computed tomography; DISH = diffuse idiopathic skeletal hyperostosis; EMG = electromyography; ES = Eagle’s syndrome; FSHD = facioscapulohumeral dystrophy; IJV = internal jugular vein; MRI = magnetic resonance imaging; NCS = nerve conduction study; SAN = spinal accessory nerve; TP = transverse process

Patients with spinal accessory nerve (SAN) palsy experience a painful shoulder with disrupted scapulothoracic rhythm and limitations in active abduction past 90°. The most common etiology is iatrogenic injury resulting from lymph node biopsy in the posterior cervical triangle.1 Other causes include intentional sacrifice during radical neck dissections, penetrating cervical trauma, acromioclavicular or sternoclavicular dislocations, and skull base or other tumors.2

Eagle’s syndrome (ES) describes the clinical presentation of dysphagia, globus sensation, and otalgia, resulting from an elongated styloid process or calcified stylohyoid ligament.3 It has not been previously reported as a cause of SAN palsy. We present the first two published case descriptions of SAN palsy resulting from compression by an angulated, hypertrophied, or calcified styloid process.

Illustrative Cases

Case 1

Clinical Presentation

A 71-year-old man presented to a multidisciplinary peripheral nerve clinic with a 2-year history of progressive unilateral weakness of his right shoulder and difficulty performing overhead tasks. He denied any preceding history of trauma, past surgical history, viral prodrome, or sudden onset of pain. Clinical examination showed right lateral scapular winging that was accentuated with shoulder abduction (Fig. 1A) and significant atrophy of the trapezius and sternocleidomastoid muscles (Fig. 1B and C). He demonstrated a positive Superman sign, with the inability to raise his right shoulder overhead while prone, resulting in a positive Triangle test.4

FIG. 1
FIG. 1

Case 1. Clinical examination demonstrating right lateral scapular winging with shoulder abduction (A) and atrophy of the right trapezius and sternocleidomastoid muscles (B) compared with the normal side (C).

Imaging

Magnetic resonance imaging (MRI) excluded the presence of a skull base tumor but did reveal compression of the internal jugular vein (IJV) by the styloid process, below the jugular foramen. Computed tomography (CT) and MRI confirmed extrinsic compression of the right IJV and SAN between the styloid process and hypertrophied transverse process (TP) of the C1 vertebrae. The styloid process measured 2.2 cm in length, which is within normal limits, and demonstrated 31° of angulation in the coronal plane.5 There was marked effacement and narrowing of the atlanto-styloid space, measuring only 1.5 mm, compared to 2.5 mm on the unaffected left side (Fig. 2). To rule out other causes of scapular winging, genetic testing was performed and was negative for facioscapulohumeral dystrophy (FSHD). This was corroborated with MRI findings of muscle volume loss in the affected trapezius muscle rather than fatty replacement of other muscles typically involved in FSHD, such as the serratus anterior, teres major, and periscapular muscles.6

FIG. 2
FIG. 2

Anatomical illustration (A) of the compression of the internal jugular vein and spinal accessory nerve between the styloid process and C1 transverse processes. Case 1. Axial oblique computed tomography (CT) (B) illustrating the proximity of the styloid (blue arrow) to the C1 transverse process (red asterisk) and effacement of the atlanto-styloid space.

Electromyography and Nerve Conduction Study

Electrophysiological testing showed abnormal motor amplitude and a reduced compound muscle action potential (CMAP) response to the upper trapezius. CMAPs were absent in the middle and lower trapezius. Needle electromyography (EMG) was abnormal with no volitional motor units and decreased insertional activity in the middle and lower trapezius. There was evidence of chronic neuropathic motor unit potentials in the upper trapezius with a large amplitude, reduced recruitment pattern, and sparse denervation.7

Management

Given the preservation of the motor units in the upper trapezius, surgical exploration, SAN decompression, and styloidectomy were suggested. The goal of surgery was to prevent further loss of trapezius motor function, given the duration of axonal loss and atrophy of more than 2 years. Surgery was performed through a transcervical neck dissection approach, with mobilization of the parotid to identify the styloid process. As suggested on imaging, the styloid process was not calcified or elongated but was angulated, leading to impingement of the SAN against the C1 transverse process (Fig. 2)

At the 6-month follow-up, the patient had improvement in pain and sleep and the ability to use the right upper limb. The EMG and nerve conduction studies (NCSs) demonstrated an increase in upper trapezius CMAP amplitude and a greater number of maturing motor units, suggestive of reinnervation to the sternocleidomastoid and upper trapezius.

Case 2

Clinical Presentation

A 61-year-old man presented to the Orthopedic Shoulder Clinic with a multiyear history of persistent left shoulder pain, after a remote prior rotator cuff repair. After attempting to lift a heavy object, he described significant pain, as well as a “tearing/ripping” sensation in his shoulder, with progressive weakness with overhead activities. This was accompanied by intermittent neck pain, odynophagia, and dysphagia.

His past medical history included diffuse idiopathic skeletal hyperostosis (DISH), which is characterized by entheseal ossification and calcification of the axial and appendicular skeleton.8 Physical examination revealed normal strength testing for the deltoid and rotator cuff muscles with no concerns for mechanical failure of his rotator cuff repair. There was marked atrophy of the sternocleidomastoid and trapezius muscles with lateral scapular winging and a positive triangle test and positive Superman sign.4 The remainder of the cranial nerve examination was normal.

Imaging

Measurements based on CT showed a left styloid process measuring 2.3 cm in length, with a coronal plane angle of 29°. There was also marked effacement of the atlanto-styloid space measuring 5.7 mm on the symptomatic left side compared to 3.7 mm on the nonsymptomatic right side. There was significant expansion and ossification of the styloid process and stylohyoid ligament causing compression of the left IJV and SAN (Fig. 3). There was progression of his DISH with extensive anterior fusion of C3–5 and C6–7, with a large anterior osteophyte at the level of C5–6, which partially explained his odynophagia. MRI excluded the presence of a skull base tumor and other extrinsic causes of SAN compression at the jugular foramen.

FIG. 3
FIG. 3

Case 2. Axial (A) and coronal (B) CT images and three-dimensional reconstruction (C) demonstrating significant expansion and ossification of the stylohyoid ligament (red asterisks).

Electromyography and Nerve Conduction Studies

Electromyography and NCSs confirmed an axonal SAN palsy with increased insertional activity, increased duration of polyphasic motor units, and reduced recruitment in the upper trapezius in keeping with a chronic axonal loss neurogenic process. Neuropathic recruitment was seen in the middle trapezius and sternocleidomastoid muscles.

Management

The patient underwent decompression of the SAN and styloidectomy through a transcervical neck dissection approach. A prominent styloid process and calcified stylohyoid ligament were removed in piecemeal fashion (Fig. 4). The hypoglossal nerve, jugular vein, and external carotid were carefully protected during the dissection down to the styloid process. The C1 transverse process was prominent, but after performing the styloidectomy, it was deemed to be no longer impinging on the SAN.

FIG. 4
FIG. 4

Intraoperative photographs of the styloid process in situ (A) and following excision (B).

At 4 months postoperatively, the patient had improved pain and shoulder mobility. Repeat electrophysiology studies demonstrated improvement in the motor amplitude to the upper and middle trapezius CMAPs and evidence of reinnervation with nascent motor units in the upper trapezius and sternocleidomastoid muscles.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Discussion

Observations

Spinal accessory nerve compression between the styloid and C1 transverse process is a rare but important diagnosis to include in the differential for SAN palsy. We suggest this compression is an atypical variant of ES, originally described by otolaryngologist W. W. Eagle.3 Eagle’s syndrome is often by characterized by otalgia, dysphagia, dysphonia, and globus sensation, which are frequently thought to occur due to an elongated or calcified styloid process.3 Other variants of ES exist, including impingement of the internal carotid artery and IJV.9–12 Peripheral nerve compression has also been reported, specifically impingement of the facial, trigeminal, glossopharyngeal, hypoglossal, and vagus nerves13–15; however, there have been no previous reports of SAN involvement.

Controversy exists as to whether an elongated styloid process is pathognomonic for ES, since 7% of the population have elongated styloid processes, which is defined as greater than 4 cm, and up to 78% have stylohyoid ligament calcifications.16 The direction of angulation and the absolute distance between the C1 TP and styloid process may be important factors determining the symptoms and structures affected.5,10,15 Medial and anterior deviation can tent against the tonsillar fossa, causing the original symptoms described by Eagle; lateral deviation can impinge the external carotid artery; and posterior deviation can compress the internal carotid artery, internal jugular vein, and spinal accessory nerve.17

In our report, case 1 had a normal styloid process length, but its slight posterior-medial deviation combined with hypertrophy of the C1 TP led to significant compression of both the IJV and SAN. Case 2 had significant calcification of the styloid and stylohyoid ligament, possibly due to extraspinal manifestations related to DISH. His odynophagia may have been partly due to a large anterior cervical osteophyte or related to direct compression of an elongated styloid process in the tonsillar fossa. His symptoms improved following styloidectomy, suggesting a tonsillar source, and may have been consistent with the traditional mechanism of dysphagia seen in ES.

Both patients’ clinical findings of lateral scapular winging accentuated in abduction and a positive triangle sign indicate trapezial dysfunction. This contrasts to the more commonly seen long thoracic nerve palsy, which is associated with medial scapular winging and a negative triangle sign. These patients do not have any difficulties with overhead shoulder forward flexion in a prone position.4 In addition, both patients had significant atrophy in both the trapezius and sternocleidomastoid muscles, indicating a proximal compression point. Advanced imaging, such as CT with three-dimensional reconstruction and MRI, was helpful in excluding other causes of extrinsic SAN compression, such as a glomus tumor or meningioma.

In these cases of SAN compression from an angulated or calcified styloid process, surgical decompression and styloidectomy led to good results with the recovery of trapezius function despite the prolonged degree of muscle atrophy. It is unclear if the patients will regain significant middle and inferior trapezius function, given the lack of motor units seen preoperatively. The fundamental principle in axonal loss nerve injuries and chronic compression is that “time is muscle.”18 Despite decompression, the potential for muscle recovery is diminished in the setting of chronic denervation, muscle atrophy, and loss of neuromuscular endplates muscle and fatty infiltration.18–20

Lessons

Compression from a posteriorly angulated or calcified styloid process can result in SAN palsy, and this can be considered an atypical winged variant of ES, named “winged” because of the associated scapular winging. This ES variant should be considered in the differential for SAN palsy as a rare, underrecognized, but important cause. Involvement of a multidisciplinary approach is needed and can include peripheral nerve surgery (neurosurgery/plastics/orthopedics), physical medicine and rehabilitation (neurophysiology), radiology, and head and neck surgery. This multidisciplinary approach is encouraged to ensure timely diagnosis, surgical success, and improved outcomes.4,21

Acknowledgments

We thank Christine Zanutto for her expertise in medical illustration.

Author Contributions

Conception and design: Miller, Wu, Yoo, Ohorodnyk, Ross. Acquisition of data: Wu, Siddiqi, Ohorodnyk. Analysis and interpretation of data: Miller, Yoo. Drafting of the article: Mitchell, Yoo, Ohorodnyk. Critically revising the article: all authors. Reviewed submitted version of the manuscript: Miller, Mitchell, Wu, Yoo, Ross. Approved the final version of the manuscript on behalf of all authors: Miller. Administrative/technical/material support: Mitchell, Yoo. Study supervision: Miller, Siddiqi, Ross.

Supplemental Information

Previous Presentations

Presented at the American Society of Peripheral Nerve Virtual Meeting ePoster January 15–21, 2021: “Winged” Eagle’s Syndrome—A Rare Cause of Spinal Accessory Nerve Palsy. Virtual meeting.

References

  • 1

    Berry H, MacDonald EA, Mrazek AC. Accessory nerve palsy: a review of 23 cases. Can J Neurol Sci. 1991;18(3):337341.

  • 2

    Sergides NN, Nikolopoulos DD, Polyzois IG. Idiopathic spinal accessory nerve palsy. A case report. Orthop Traumatol Surg Res. 2010;96(5):589592.

  • 3

    Eagle WW, Elongated styloid process: further observations and a new syndrome. Arch Otolaryngol. 1948;47(5):630592.

  • 4

    Macaluso S, Ross DC, Doherty TJ, Doherty CDMT, Miller TA. Spinal accessory nerve injury: a potentially missed cause of a painful, droopy shoulder. J Back Musculoskeletal Rehabil. 2016;29(4):899904.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Burulday V, Akgül MH, Bayar Muluk N, Yağdiran B, Inal M. The importance of medial-lateral styloid process angulation/coronal plane angle in symptomatic eagle syndrome. Clin Anat. 2017;30(4):487491.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Gerevini S, Scarlato M, Maggi L, et al. Muscle MRI findings in fascioscapulohumeral muscular dystrophy. Eur Radiol. 2016;26:693705.

  • 7

    Green RFBM, Brien M. Accessory nerve latency to the middle and lower trapezius. Arch Phys Med Rehabil. 1985;66(1):2324.

  • 8

    Mader R, Verlaan JJ, Eshed I, et al. Diffuse idiopathic skeletal hyperostosis (DISH): where we are now and where to go next. RMD Open. 2017;3(1):e000472.

  • 9

    Zamboni P, Scerrati A, Menegatti E, et al. The Eagle jugular syndrome. BMC Neurol. 2019;19(1):333.

  • 10

    Mantovani G, Zangrossi P, Flacco ME, et al. Styloid jugular nutcracker: the possible role of the styloid process spatial orientation—a preliminary morphometric computed study. Diagnostics (Basel). 2023;13(2):298.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Dashti SR, Nakaji P, Hu YC, et al. Styloidogenic jugular venous compression syndrome: diagnosis and treatment: case report. Neurosurgery. 2012;70(3):E795E799.

  • 12

    Radak D, Tanaskovic S, Kecmanovic V, Babic S, Popov P, Gajin P. Bilateral Eagle syndrome with associated internal carotid artery kinking and significant stenosis. Ann Vasc Surg. 2016;34:271.e15271.e18.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    Rosales N, Gandhi R LR. Rare presentation of Eagle’s syndrome as Bell’s palsy. Neurology2. 14AD;82(10 suppl):P7.023.

  • 14

    Bedajit RK, Priyokumar O, Abhilash RKS. Eagle syndrome with multiple cranial nerve involvement. J Med Soc. 2014;228(2):117119.

  • 15

    Ho S, Luginbuhl A, Finden S, Curry JM, Cognetti DM. Styloid/C1 transverse process juxtaposition as a cause of Eagle’s syndrome. Head Neck. 2015;37(11):E153E156.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Costantinides F, Vidoni G, Bodin C, Di Lenarda R. Eagle’s syndrome: signs and symptoms. Craniomandib Sleep Pract. 2013;31(1):5660.

  • 17

    Piagkou M, Anagnostopoulou S, Kouladouros K, Piagkos G. Eagle’s syndrome: a review of the literature. Clin Anat. 2009;22(5):545558.

  • 18

    Kobayashi J, Mackinnon SE, Watanabe O, Ball DJ, Gu XM, Hunter DA. The effect of duration of muscle denervation on functional recovery in the rat model. Muscle Nerve. 1998;20(7):858866.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Barnes SL, Miller TA, Simon NG. Traumatic peripheral nerve injuries: diagnosis and management. Curr Opin Neurol. 2022;35(6):718727.

  • 20

    Yoshimura K, Asato H, Jejurikar SS, Cederna PS, Urbanchek MG, Kuzon WM Jr. The effect of two episodes of denervation and reinnervation on skeletal muscle contractile function. Plast Reconstr Surg. 2002;109(1):212219.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 21

    Seror P, Stojkovic T, Lefevre-Colau MM, Lenglet T. Diagnosis of unilateral trapezius muscle palsy: 54 cases. Muscle Nerve. 2017;56(2):215223.

  • Collapse
  • Expand
  • FIG. 1

    Case 1. Clinical examination demonstrating right lateral scapular winging with shoulder abduction (A) and atrophy of the right trapezius and sternocleidomastoid muscles (B) compared with the normal side (C).

  • FIG. 2

    Anatomical illustration (A) of the compression of the internal jugular vein and spinal accessory nerve between the styloid process and C1 transverse processes. Case 1. Axial oblique computed tomography (CT) (B) illustrating the proximity of the styloid (blue arrow) to the C1 transverse process (red asterisk) and effacement of the atlanto-styloid space.

  • FIG. 3

    Case 2. Axial (A) and coronal (B) CT images and three-dimensional reconstruction (C) demonstrating significant expansion and ossification of the stylohyoid ligament (red asterisks).

  • FIG. 4

    Intraoperative photographs of the styloid process in situ (A) and following excision (B).

  • 1

    Berry H, MacDonald EA, Mrazek AC. Accessory nerve palsy: a review of 23 cases. Can J Neurol Sci. 1991;18(3):337341.

  • 2

    Sergides NN, Nikolopoulos DD, Polyzois IG. Idiopathic spinal accessory nerve palsy. A case report. Orthop Traumatol Surg Res. 2010;96(5):589592.

  • 3

    Eagle WW, Elongated styloid process: further observations and a new syndrome. Arch Otolaryngol. 1948;47(5):630592.

  • 4

    Macaluso S, Ross DC, Doherty TJ, Doherty CDMT, Miller TA. Spinal accessory nerve injury: a potentially missed cause of a painful, droopy shoulder. J Back Musculoskeletal Rehabil. 2016;29(4):899904.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Burulday V, Akgül MH, Bayar Muluk N, Yağdiran B, Inal M. The importance of medial-lateral styloid process angulation/coronal plane angle in symptomatic eagle syndrome. Clin Anat. 2017;30(4):487491.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Gerevini S, Scarlato M, Maggi L, et al. Muscle MRI findings in fascioscapulohumeral muscular dystrophy. Eur Radiol. 2016;26:693705.

  • 7

    Green RFBM, Brien M. Accessory nerve latency to the middle and lower trapezius. Arch Phys Med Rehabil. 1985;66(1):2324.

  • 8

    Mader R, Verlaan JJ, Eshed I, et al. Diffuse idiopathic skeletal hyperostosis (DISH): where we are now and where to go next. RMD Open. 2017;3(1):e000472.

  • 9

    Zamboni P, Scerrati A, Menegatti E, et al. The Eagle jugular syndrome. BMC Neurol. 2019;19(1):333.

  • 10

    Mantovani G, Zangrossi P, Flacco ME, et al. Styloid jugular nutcracker: the possible role of the styloid process spatial orientation—a preliminary morphometric computed study. Diagnostics (Basel). 2023;13(2):298.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Dashti SR, Nakaji P, Hu YC, et al. Styloidogenic jugular venous compression syndrome: diagnosis and treatment: case report. Neurosurgery. 2012;70(3):E795E799.

  • 12

    Radak D, Tanaskovic S, Kecmanovic V, Babic S, Popov P, Gajin P. Bilateral Eagle syndrome with associated internal carotid artery kinking and significant stenosis. Ann Vasc Surg. 2016;34:271.e15271.e18.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    Rosales N, Gandhi R LR. Rare presentation of Eagle’s syndrome as Bell’s palsy. Neurology2. 14AD;82(10 suppl):P7.023.

  • 14

    Bedajit RK, Priyokumar O, Abhilash RKS. Eagle syndrome with multiple cranial nerve involvement. J Med Soc. 2014;228(2):117119.

  • 15

    Ho S, Luginbuhl A, Finden S, Curry JM, Cognetti DM. Styloid/C1 transverse process juxtaposition as a cause of Eagle’s syndrome. Head Neck. 2015;37(11):E153E156.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Costantinides F, Vidoni G, Bodin C, Di Lenarda R. Eagle’s syndrome: signs and symptoms. Craniomandib Sleep Pract. 2013;31(1):5660.

  • 17

    Piagkou M, Anagnostopoulou S, Kouladouros K, Piagkos G. Eagle’s syndrome: a review of the literature. Clin Anat. 2009;22(5):545558.

  • 18

    Kobayashi J, Mackinnon SE, Watanabe O, Ball DJ, Gu XM, Hunter DA. The effect of duration of muscle denervation on functional recovery in the rat model. Muscle Nerve. 1998;20(7):858866.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Barnes SL, Miller TA, Simon NG. Traumatic peripheral nerve injuries: diagnosis and management. Curr Opin Neurol. 2022;35(6):718727.

  • 20

    Yoshimura K, Asato H, Jejurikar SS, Cederna PS, Urbanchek MG, Kuzon WM Jr. The effect of two episodes of denervation and reinnervation on skeletal muscle contractile function. Plast Reconstr Surg. 2002;109(1):212219.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 21

    Seror P, Stojkovic T, Lefevre-Colau MM, Lenglet T. Diagnosis of unilateral trapezius muscle palsy: 54 cases. Muscle Nerve. 2017;56(2):215223.

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