Abstract
Background and Purpose There are few reports in the literature of adverse effects resulting from massage therapy (MT) and no reports of brachial plexus injury (BPI) associated with MT. This case report describes an uncommon case of BPI that developed after a session of MT and reviews previously published reports of peripheral nerve injury following MT.
Case Description A 58-year-old Asian woman developed sudden unilateral paralysis of her left shoulder girdle after a session of MT. A diagnosis of acute BPI was suspected due to her recent history and the results of several examinations. The results of electrodiagnostic studies indicated a possible location for the lesion and ultimately led to a different diagnosis.
Outcomes The patient regularly participated in a twice-weekly rehabilitation program targeting the left shoulder. The rehabilitation program included supervised passive range of motion, strengthening, and stretching exercises as well as a home exercise program. A 12-month follow-up showed the patient had achieved gradual recovery of shoulder strength, resolution of limitations of range of motion, and relief of shoulder pain.
Discussion This is believed to be the first report of BPI associated with MT. This case report serves as a reminder to massage therapists and physical therapists that MT of the neck should be carefully performed to avoid injury. Further studies will help design safer and more effective MT for the future.
The brachial plexus is a network of nerves that originate in the spine and is formed by the ventral rami of the lower 4 cervical and first thoracic nerve roots.1 From the spine, the cervical and thoracic nerve roots travel between the anterior and middle scalene muscles and divide into 3 trunks in the posterior cervical triangle, traveling through the neck, the axillary region, and into the arm.
Brachial plexus injury (BPI), which affects approximately 1.2% of patients worldwide, is caused by damage to the cervical and thoracic nerves.1 This injury typically results from excessive stretching (usually from traffic accident–related traction and compression of the nerves), humeral fracture, penetrating injuries, neoplasms, radiation treatment, or participation in contact sports.2
Brachial plexus injury can induce severe neurologic deterioration, leading to paralysis of the arm and hypothesia, which can interrupt daily activities and function. Thus, clinicians need to be aware of the possible mechanisms of injury and should attempt to pinpoint the location of injury in order to plan the best therapeutic strategy. Diagnosis and management of BPI can be challenging, especially when the mechanism of nerve injury is unusual.
Diagnostic methods include a detailed clinical evaluation combined with radiological and electrodiagnostic assessment. Electrodiagnostic evaluation plays an important role in helping determine the severity and location of the injury and the possible prognosis.3 Depending on the mechanism of trauma and the degree of nerve injury, BPI can be treated with 3 main methods: surgical repair, medication, and rehabilitation. In this article, we report an uncommon case of BPI that developed after a session of massage therapy (MT). We also review other complications resulting from MT that have been discussed in the literature. The purpose of presenting this case report is to remind massage therapists and physical therapists that MT of the neck should be carefully performed to avoid injury.
Case Description
A 58-year-old, right-handed Asian woman came to our emergency department with severe pain and weakness in her left shoulder after she had received MT. The patient worked as a housekeeper, and her job usually involved only light physical work. Two years before her visit to our emergency department, she had a severe fall, during which she fractured her left distal radius. Open reduction and internal fixation of her left radius and insertion of a buttress plate were performed shortly after her injury. She also had a painful sensation in her left shoulder and found it hard to extend her arm over her head. Musculoskeletal ultrasonography of her left shoulder revealed small full-thickness tears of the supraspinatus tendon, combined with signs of impingement between a coracoacromial ligament and the greater tuberosity of the humerus. Acromioplasty and surgical repair were done 3 months later. After surgery, she had a good recovery and again could independently perform her daily activities. Her only remaining symptom was mild numbness of her left hand.
The patient told us that she had recently received periodic MT in her nuchal and shoulder regions to relieve mild myofascial pain. She received the deep tissue massage while she was seated upright in a chair. The massage sessions usually lasted from 45 to 60 minutes and were scheduled twice a week, depending on her request. She had undergone a total of 4 MT sessions when her symptoms appeared. The patient reported having no post-massage discomfort until 2 days before visiting our emergency department. During the last session of MT, she felt sudden weakness and numbness of her left shoulder and recalled that she had felt deeper compression than before at the posterior triangle of her neck (Fig. 1). She also reported that as the day progressed, her symptoms worsened and she had developed sudden paralysis of her left shoulder girdle. The paralysis was accompanied by severe pain on the second day after the massage.
Brachial plexus in the posterior triangle of the neck. Red color of upper trunk indicates possible injury site.
Clinical Impression 1
Our first step was to evaluate the sudden onset of monoplegia in order to determine whether there was sensory involvement (Fig. 2). For example, the myopathy was not likely to be due to sudden unilateral monoplegia with sensory involvement without muscle atrophy and fasciculation. Our patient had sensory-involved symptoms, so the neuropathy appeared to be the lesion causing unilateral monoplegia. The neuropathy involved the central and peripheral nervous systems. The potential differential diagnosis relative to upper motor neuron signs includes cardiovascular diseases, spinal cord injury, and so on. The conditions or diseases relative to the lower motor neuron include brachial plexus injury, cervical radiculopathy, suprascapular neuropathy, infection (Parsonage-Turner syndrome), and so on.4 The second step was to determine and differentiate upper or lower motor neuron lesions. In clinical practice, upper motor neuron disorders involving a paralyzed arm include signs of hyperactive tendon reflexes or possibly the Hoffmann sign. In contrast, decreased tendon reflexes, or muscle weakness or wasting, imply lower motor neuron involvement.
Approach to the diagnosis of limb weakness.
After we evaluated the patient's history and clinical symptoms, infection or tumor were excluded because there was no history of migraine headaches, recent fever, weight loss, seizures, facial palsy, skin lesions, or any specific underlying disease.
Examination
Physical examination revealed left upper arm paralysis (muscle power grade was 2, which equals active movement with gravity eliminated) and hypothesia involving the deltoid (shoulder abduction), biceps (elbow flexion), and triceps (elbow extension) muscles. The flexion and extension of the wrist and fingers were essentially normal. The deep tendon reflexes of the left biceps (main C5) and brachioradialis (main C6) tendons were decreased but otherwise were normal. The active range of motion (ROM) of the neck and passive ROM of the left shoulder joint were normal. Radiation of pain from the left side of the neck to the shoulder region could be elicited by percussing Erb's point, and no significant signs occurred with the Spurling test for cervical root signs. There was no other neurological deficit, such as cranial nerve dysfunction, dysarthria, or incontinence.
The results of blood tests, including complete blood count and electrolyte and metabolic profiles, were normal. Computed tomography of the brain revealed no evidence of intracranial hemorrhage or territory infarction, but musculoskeletal ultrasonography of the left shoulder showed mild tenosynovitis of the bicipital tendon. In addition, magnetic resonance imaging of the neck revealed herniated intervertebral disk disease of the cervical spine at the C3–C6 level, with mild compression of the bilateral spinal cord at the C3–C4 level. According to the physical examination and image findings, the cervical radiculopathy or BPI should be taken into consideration.
To confirm the diagnosis, we ordered nerve conduction studies and electromyography (EMG) 4 weeks after the onset of symptoms. The timing was important because such denervations occur after Wallerian degeneration, at around 9 to 11 days.5 Generally, the abnormal spontaneous denervation potentials (fibrillation potentials and positive sharp wave) would be evident on EMG 10 to 14 days after the onset of peripheral nerve injury in proximal muscles and as late as 21 to 30 days in distal muscles.6 The huge fibrillation potentials and positive sharp wave (>100 μV) implied a recent denervation.7 The antidromic nerve conduction studies were performed according to the American Academy of Neurology protocol.8 The results of the nerve conduction studies revealed decreased conduction velocity of the sensory nerve action potential of the left median, radial, and ulnar nerves. The median and ulnar motor nerves were normal. Electromyography of the left biceps, triceps, deltoid, and supraspinatus muscles revealed increased fibrillation potentials and positive sharp waves, along with reduced recruitment and an interference pattern affecting the motor unit action potential (Tab. 1). Furthermore, the EMG results showed no signs of abnormal denervation in the cervical paraspinal, first dorsal interosseous, and abductor pollicis brevis muscles.
Baseline Nerve Conduction and Electromyography Studiesa
Clinical Impression 2
The findings from the nerve conduction studies and EMG showed denervation with renervation in the biceps, triceps, deltoid, and supraspinatus muscles (in the territory of the brachial plexus nerve) and absence of denervation of C5 and C6 paraspinal muscles (the root level). Moreover, physical examination showed paralysis of the left deltoid, biceps, and triceps muscles and decreased tendon reflexes of the biceps and brachioradialis, which was compatible with the electrodiagnostic results. All of these findings pointed to a diagnosis of recent brachial plexopathies, predominantly involving the upper trunk (Tab. 2).2 In addition, the severity of brachial plexopathies was described as second-degree peripheral nerve injury, or axontomesis (disruption of the neuronal axon but with maintenance of the myelin sheath), according to Seddon's classification.9
Anatomy of Innervated Muscles and Denervation Signs on Electromyography (EMG) in the Present Casea
Outcome
The patient regularly participated in a twice-weekly rehabilitation program targeting the left shoulder. The program included supervised passive ROM exercises and strengthening and stretching exercises as well as a home exercise program. Significant improvements in ROM and visual analog scale pain scores for the left shoulder were found on follow-up at 3, 6, 9, and 12 months. The patient's muscle power grade increased from 2 to 4, and gradual improvement was noted at the 12-month follow-up. The tendon reflexes in the biceps and brachioradialis also recovered to near normal.
The patient's rehabilitation program is ongoing, and her symptoms have gradually lessened so that she is once more able to perform regular activities of daily living without assistance. The follow-up EMG at 12 months showed increased polyphasic potentials with higher amplitude, without abnormal denervation in the biceps, triceps, supraspinatus, and deltoid muscles. This finding indicated progressive reinnervation after denervation (Tab. 3).
Results of Nerve Conduction and Electromyography Studies at 12-Month Follow-upa
Discussion
Four previous case reports have shown nerve injury associated with MT,10–13 but, to our knowledge, this is the first report of BPI associated with MT (Tab. 4). Herskovitz et al10 reported the case of a patient with mononeuropathy of the median recurrent motor branch that elicited by manual compression. Giese and Hentz11 described a patient who developed posterior interosseous syndrome after deep tissue massage of the forearm; 3 weeks later, the patient had nearly full recovery. The authors concluded that the nerve is more vulnerable to a compressive injury when in a relatively immobile and nondistensible space. Aksoy et al12 described a patient with spinal accessory neuropathy following deep tissue massage; this patient had incomplete recovery of muscle strength with total pain relief after 2 years of follow-up. Wu et al13 reported on a patient with posterior interosseous nerve palsy that followed friction massage. Our patient developed nerve injury after MT, and this is the first post-MT BPI report in the literature. Other complications resulting from MT include renal artery embolization,14 ureteral stent displacement,15 hepatic hematoma,16 retinal and cerebral artery embolism,17 cervical cord injury,18 and others.19,20
Summary of Previously Published and Present Cases of Peripheral Nerve Injury Following Massage Therapy
The mechanism of nerve injury from MT is unusual. We believe the possible mechanism for this injury, as in our case and in previous cases, was associated with direct and vigorous pressure at Erb's point during MT, causing compressive injury of the brachial plexus. Ross et al21 reported persistent weakness of the shoulder after rotator cuff tendon repair. The other possible contributing factor might be the deconditioning of our patient's left shoulder muscles and surrounding soft tissue, compared with her unaffected right shoulder, due to the acromioplasty and tendon repair 2 years previously. Hence, less protection and support for the brachial plexus might contribute to greater compressive injury.
The nerve conduction studies and EMG played an important role in making the diagnosis of brachial plexopathy, including assessment of severity and localization of the lesion.2 The EMG in our case demonstrated many fibrillation potentials and positive sharp waves in the biceps, deltoid, and supraspinatus muscles. In contrast, the cervical paraspinal muscle was spared (Tab. 1). This finding could indicate that the injury occurred at the upper trunk instead of the root of the cervical nerve. The spontaneous potentials found at the triceps muscle on EMG also suggested that the middle trunk of the brachial plexus might be involved. However, we did not survey the flexor carpi radialis, pronator teres, or extensor carpi radialis muscles (middle trunk territory); thus, it was difficult to differentiate the damaged lesion from the middle trunk.
Successful management of BPI depends on the type of lesion, its location, the degree of severity, and the duration of the injury.6,22 Conservative treatment has been the first approach for patients with nerve continuity (eg, neuropraxia, axontomesis). For example, rehabilitation could reduce early and long-lasting disability (ROM limitation, joint contracture, and secondary deformities),23 and drug therapy, therapeutic ultrasound, or transcutaneous electrical nerve stimulation might relieve neuropathic pain. In contrast, surgical intervention (eg, graft repair, motor nerve transfers, neurotization procedures) should be recommended in patients without evidence of reinnervation at 3 months postinjury or those who respond poorly to conservative treatment.24
The prognosis for BPI varies and depends on the location, type, and severity of injury.22 Recovery after neurapraxia (demyelination with intact nerve structure) is usually good, and patients have 90% to 100% return of function. The recovery starts within 2 to 3 weeks after the injury and is always complete within 6 to 8 weeks. The prognosis of axonotmesis is usually fair to good, and the rate of recovery depends on the distance from the site of injury (axonal regeneration of 1–4 mm per day). People with neurotmesis (both axon and encapsulating connective tissue lose their continuity) often have a poor prognosis and always need surgical intervention. Both the clinical symptoms and electrophysiological results of the present case, indicating fair to good functional recovery, were similar to previous cases of axonotmesis.
Massage therapy involves manual manipulation of soft tissue and is designed to relieve discomfort such as low back pain as well as to alleviate anxiety and depression. Massage therapy has long been included as part of the complementary and alternative medical therapies in many countries, and its benefits are well known.25 The mechanism for pain relief after MT has been shown to be related to decreased levels of the neuropeptide substance P.26 However, few complications associated with MT have been reported, and our case was a reminder that massage therapists need to carefully treat areas over nerves, vessels, and internal devices. Moreover, massage training should include sections on muscular anatomy and the nervous system, which will help avoid further nerve injury.
This case, which we believe is the first case of BPI resulting from MT, serves as a reminder to massage therapists and physical therapists that MT of the neck should be carefully performed. Further studies will help design safer and more effective MT in the future.
Footnotes
Dr C-Y Chang, Dr Chiang, and Dr Chen provided concept/idea/study design. Dr C-Y Chang and Dr Chiang provided writing. Dr Chan and Dr Wu provided data analysis. Dr C-Y Chang, Dr Chan, Dr Wu, Dr Chen, and Dr S-T Chang provided consultation (including review of the manuscript before submission).
- Received October 25, 2013.
- Accepted August 28, 2014.
- © 2015 American Physical Therapy Association
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