This case report was approved by Institutional Review Board of Wooridul Spine Hospital and consent was obtained by the patient. Dorsal scapular neuropathy (DSNP) is caused by neural entrapment due to a hypertrophic middle scalene muscle, stretching of the dorsal scapular nerve (DSN) during traumatic movements, or direct iatrogenic and accidental injury [1-3].

The DSN mainly originates from the C5 spinal nerve. It pierces the middle scalene muscle and travels posteriorly between the serratus posterior superior and levator scapulae muscles to innervate the rhomboid major, minor and, occasionally, the levator scapulae [4]. Rhomboid major and minor functions to retract, elevate and stabilize the scapula during shoulder motion [5]. Thus the DSNP produces paralysis of rhomboids and levator muscles, which manifests as shoulder or scapular pain, weakness of right shoulder abduction, or winged scapular. But this condition is rarely occurred and frequently underdiagnosed, because inability of arm elevation and shoulder pain frequently lead the physicians to suspect the cervical and shoulder problems, rather than isolated weakness of rhomboids and levator scapulae from DSNP [6].

DSPN usually manifests as shoulder and scapular pain, which is clue to approach this diagnosis. But the patient in this case did not have complained of shoulder and scapular pain so that he had been treated by wrong way for a long time since misdiagnosis had been made. To make exact diagnosis by excluding other diseases manifested as similar clinical symptoms to DSNP is important key to choose appropriate treatment method. Recently, we experienced case of the male patient presented with difficulty of right arm elevation and diagnosed as DSNP through careful clinical examination and electrodiagnostic study and hereby presented this case report.

A 23-year-old man was admitted to department of physical and rehabilitation medicine with chief complaint of 2-year history of difficulty of right shoulder abduction. He stated that this condition had been abruptly developed when he had lifted heavy objects upward for exercise of shoulder girdle muscles. He had experienced no pain around right shoulder at that time and thereafter. He denied any episode of febrile illness or gastrointestinal disturbance suggesting viral infection at several days before beginning of this condition. He brought the magnetic resonance image (MRI) of right shoulder, taken about one and half year before in another hospital for evaluation of shoulder lesion. This revealed partial tear of right supraspinatus tendon. He had undergone physical therapy and injection treatment around right shoulder until then, but his main complaint was not recovered at all. There was no notable family history suggesting genetic disorder.

Physical examination on cervical spine revealed no pain on neck extension and flexion, negative spurling sign, and no significant tenderness on muscles around neck and shoulder. No positive sign was found on shoulder impingement or apprehension test, and there were no acromioclavicular, bicipital, or subacromial tenderness. Passive range of motion (ROM) of right shoulder flexion and abduction was full, whereas active abduction and flexion of right shoulder was limited and especially was difficult to initiate. Muscle strength of shoulder abductor and flexor was preserved to have the ability to resist examiner’s counterforce. Muscle strength of muscle groups other than shoulder girdle muscles was measured as normal grade. Muscle tone of right upper extremity was normal, deep tendon reflex was normoactive, and no pathologic reflex such as Hoffmann sign was found. No abnormal sensory function was observed on right upper extremity. On inspection, right scapular was more laterally located than left side, and lower medial border and inferior angle of the right scapula was more prominent as compared with the left side (Fig. 1A). In addition, this was markedly accentuated by active shoulder flexion and abduction (Fig. 1B, C).

Figure 1. Right scapular is more laterally located than left side (A), and medial border of right scapula is more markedly accentuated by active shoulder abduction (B) and flexion (C).

MRI of the cervical spine were additionally performed in our hospital, which revealed no significantly abnormal result except the suspicious finding of hypertrophied right middle scalene at C5-6 level. In electrodiagnostic test, recordings obtained from the needle electrode at the right rhomboid muscle on the stimulation of Erb point showed decreased amplitude of compound motor action potential of right dorsal scapular nerve compared with the left (1.0 mV vs. 1.7 mV). Other upper-extremity motor and sensory nerve conduction studies were normal. Needle electromyography of the right rhomboid and levator scapulae muscle revealed abnormal spontaneous activity at rest and long duration polyphasic motor unit potential and decreased recruitment of motor unit potentials at minimal to moderate degree of active contraction. A reduced interference pattern was also present on maximal contraction. Electromyography of other muscles including cervical paraspinalis, trapezius, deltoid, serratus anterior, biceps brachii, triceps brachii, brachioradialis, and flexor carpi radialis showed no abnormal findings. Taken all of these findings, the patient was diagnosed as right DSNP involving axonal component.

Rehabilitation program was performed consisting of active assistive and passive ROM exercise, muscle strengthening exercise, and scapular stabilizing exercise. Three months after the treatment program, the ability of right shoulder elevation was restored substantially and winged scapular was reduced in intensity.

DSNP is frequently delayed diagnosed or misdiagnosed because the clinical presentation may mimic or overlap other various cervical or shoulder disease. The patient in this case had been also misdiagnosed as impingement syndrome or supraspinatus tendinitis and had been treated for this condition for about 2 years, even though he did not have experienced pain on shoulder area. Our case report was distinguished from other reports that had been published, by the fact that this patient was diagnosed as DSNP without pain around shoulder and interscapular area, which was frequently encountered symptom and therefore, strong clues to approach exact diagnosis.

Difficulty in active flexion or abduction of the shoulder is main presenting clinical manifestation of DSNP. Evaluation of passive ROM of shoulder is essential. If passive ROM is full range, adhesive capsulitis can be excluded because this is characterized as restriction of active and passive ROM [7]. When active ROM is restricted without limitation of passive PROM and especially, shoulder pain is associated with arm elevation, diagnosis of rotator cuff disease or impingement syndrome is probably made, which can be ascertained by positive impingement sign [8]. But if no positive finding is observed in impingement test without limitation of passive ROM, various neuromuscular disorders should be considered. When there is no sign or symptoms suggesting upper motor neuron disease such as increased deep tendon reflex or positive pathologic reflex, the physicians can exclude possibility of upper motor neuron disease such as spinal cord lesion, and should consider the possibility of motor neuron disease, radiculopathy, neuropathy or myopathy.

Cervical radiculopathy or brachial plexopathy is usually suspected, because difficulty of shoulder abduction and flexion is observed in severe axonal pathology of C5 and C6 root, upper trunk or lateral cord [9]. Because C5 and C6 root, upper trunk or lateral cord also innervates elbow flexor muscle group such as biceps brachii, weakness of elbow flexion is required for diagnosis for radiculopathy or plexopathy [8,10]. When strength of elbow flexion is not weakened, physicians can consider the peripheral neuropathy involving axillary nerve, suprascapular nerve, dorsal scapular nerve, spinal accessory nerve, or long thoracic nerve. Among them, axillary neuropathy produces more prominent weakness of shoulder abduction in arm internal rotation, because axillary nerve innervates deltoid muscle, primary shoulder abductor [11]. On the contrary, other neuropathies involving dorsal scapular nerve, spinal accessory nerve, or long thoracic nerve, are manifested as relative preservation of shoulder abduction strength, instead, showing difficulty of initiation of shoulder abduction and presence of winged scapulae.

In this regard, careful examination and history taking help to make an approach to diagnosis of DSNP as well as differential diagnosis from other pathologies. But for exact confirmation of diagnosis and exclusion of other pathologic conditions of myopathy or other peripheral nerves than DSN, electrodiagnostic study including needle electromyography is needed. In addition, electrodiagnostic study can provide the information whether axon is damaged, which is important prognostic factor.

The summary of the male patient in this case was as follows; full passive shoulder ROM, limitation of active shoulder abduction, negative impingement test, no significant pain, no upper motor neuron sign on physical exam, and preservation of elbow flexor muscle strength. In addition, muscle strength of shoulder abductor was preserved to be able to resist examiner’s counterforce. Instead, he showed difficulty of initiating active shoulder movement and winged scapular, which was remarkably visible during shoulder abduction and flexion. These clinical findings helped us to suspect the possibility of peripheral neuropathy involving dorsal scapular nerve, spinal accessory nerve, or long thoracic nerve. Cervical and shoulder lesions could be entirely excluded by the results of cervical and shoulder MRI in addition to clinical examinations. Electrodiagnostic study provided us with useful results to exclude myopathy, radiculopathy, brachial plexopathy, and other peripheral neuropathies manifested as winged scapulae as well as to make confirmation of DSNP with the conditions of axonal involvement of branches innervating rhomboides and levator scapulae.

We did not make sure the mechanism that had caused DSNP two years before visit to our hospital. He suddenly felt difficulty of right shoulder elevation during overhead lifting exercise. This seemed not to be related to infection or immunological etiology. Needle electromyography revealed abnormal spontaneous activity both in rhomboids and levator scapulae, which meant that DSN might be entrapped proximal to the branch of levator scapulae [4]. It was assumed that DSN was entrapped in middle scalene muscle, through which nerve existed into medial border of scapular. Cervical MRI showed the suspicious findings of hypertrophied right middle scalene muscle in comparison with left side, which supported our assumption, but this was not definitely determined by radiologists. One report introduced similar case of 52 years old male who visited with weakness of right arm elevation that had been abruptly developed after lifting a heavy box overhead. This case report suggested probable mechanism as entrapment of DSN in middle scalene, which was inferred by the circumstances that symptoms occurred [12]. The case reports regarding DSNP explained that DSNP could result from traction injury from hypertrophied middle scalenus muscle during exercises of neck flexion, heavy shoulder raises, or repetitive overhead activity related to work and sports activities. [13,14]

DSNP was one of pathologic conditions presenting difficulty of arm elevation. Even though the patients did not complain of shoulder or interscapular pain, the possibility of DSNP should be considered and assessed by careful examination, radiological and electrodiagnostic studies, which might help to make exact diagnosis that may eventually lead to appropriate treatment plan.

No potential conflict of interest relevant to this article was reported.