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© 1996 The Journal of Bone and Joint Surgery, Inc. Parsonage-Turner Syndrome (Acute Brachial Neuritis)*  , INDIANAPOLIS, INDIANAInvestigation performed at the Methodist Sports Medicine Center, Indianapolis
The cases of seven patients who had had acute brachial neuritis (Parsonage-Turner syndrome) were reviewed retrospectively. The patients had been followed for a mean of six years (range, three to ten years) after the onset of the symptoms. All patients had had an acute onset of intense pain in the shoulder without antecedent trauma. The pain decreased spontaneously and eventually resolved completely in all patients. Weakness in the shoulder had developed at a mean of approximately four weeks after the initial onset of pain. The weakness decreased spontaneously but very gradually in all patients; three patients had persistent, mild weakness at the most recent follow-up evaluation.
Brachial neuritis, often referred to as Parsonage-Turner syndrome, can be a vexing problem for both the patient and the physician3-5,8-12. The characteristic symptoms—a sudden onset of severe pain in or about the shoulder girdle, followed shortly thereafter by weakness of at least one of the muscles about the shoulder—can be confused with a number of disorders. These disorders include abnormalities of the rotator cuff, acute calcific tendinitis, adhesive capsulitis, cervical spondylosis, and neurological conditions such as peripheral-nerve compression, tumor, acute poliomyelitis, and amyotrophic lateral sclerosis1,3-5,7. Although patients who have brachial neuritis are often seen and cared for by an orthopaedic surgeon, there are few studies of this disorder in the orthopaedic literature1,2,12. The purpose of the current study was to review our experience with a series of seven patients who had Parsonage-Turner syndrome.
More than 6500 patients were seen by the senior one of us (G. W. M) for problems related to the shoulder between 1985 and 1992. The cases of all patients who had been seen because of symptoms that were consistent with a diagnosis of Parsonage-Turner syndrome were reviewed retrospectively for this study. The criteria for inclusion consisted of a sudden onset of severe pain in or about the shoulder girdle without antecedent trauma, no systemic disorder that might affect the musculoskeletal system, and an onset of weakness in the involved shoulder within a few weeks after the onset of the pain. In addition, the pain and weakness had to have decreased spontaneously and electromyographic studies had to have demonstrated findings (fibrillation potentials and positive waves) that were consistent with brachial neuritis. Also, the patient had to have been followed for a minimum of two years since the time of the evaluation. Patients were excluded from the study if they had had a primary disorder of the shoulder or the cervical spine. Such disorders included abnormalities of the rotator cuff, cervical spondylosis, herniation of a disc, syringomyelia, and peripheral neuromuscular disorders. Patients also were excluded if they had noted an insidious onset of pain or weakness in the shoulder but had not had some improvement within three months, or if abnormalities due to spinal or nerve-root disorders had been detected on electromyographic testing. Fourteen patients were diagnosed with brachial neuritis during the time-period of this study, but seven of them were excluded. One of these seven patients had met all of the clinical criteria and had had electromyographic evidence of brachial plexopathy, but he had died of unrelated causes before the minimum two-year follow-up. The remaining six patients had a history and symptoms that were suggestive of Parsonage-Turner syndrome, but all were improving rapidly at the time of the initial examination at our facility and, therefore, no electromyography or other workup was performed. This left a total of seven patients who met all of the criteria for inclusion in the study. The mean age of the seven patients at the time of presentation was thirty-five years (range, sixteen to fifty-nine years). All patients were male, and all were right-hand-dominant. The dominant right upper extremity was affected in six patients. All patients were in good health, with no history of current or pre-existing systemic disorders or neurological abnormalities. No patient was involved in strenuous overhead sports. All seven patients had symptoms in the shoulder girdle that were thought, by the patient or the referring physician, to be of musculoskeletal origin. The onset of the pain had been acute and intense: three patients had been awakened at night by severe pain, and the other four had had a rapid onset of severe pain during the day. Because of the severity of the initial pain, three patients had sought treatment in the emergency department of their local hospital at the time of the onset and had been given narcotics parenterally. Four patients had ill defined, diffuse pain about the shoulder. In addition, one patient had pain that extended from the neck to the posterolateral aspect of the shoulder, and another reported pain over the superolateral aspect of the shoulder. The remaining patient had vague, diffuse pain about the shoulder along with discomfort that extended down the extremity to the forearm; this was the only patient who had paresthesias in the extremity, and he was found to have widespread involvement of the brachial plexus. Only one patient was referred for neurological consultation; he was the first patient in the current series to be seen. All patients were evaluated with serological testing (including a complete blood-cell count, determination of the Westergren erythrocyte sedimentation rate, and a blood-chemistry profile), radiographs of the shoulder and neck, and electromyography. One patient who had involvement of the suprascapular nerve was initially evaluated with an arthrogram to rule out a tear of the rotator cuff. Treatment for all patients consisted of analgesics as needed, physical therapy, and rehabilitation exercises. Because the pain resolved spontaneously, modalities such as ultrasound and cryotherapy were not needed. Physical therapy was focused on the maintenance of the range of motion of the shoulder and on the restoration of strength. All patients participated in a home-exercise program that was designed to strengthen the rotator cuff and the scapular stabilizing muscles. No patient had regular treatment by a physical therapist. No regular schedule for the timing of follow-up visits was used. Patients tended to be seen more often if the symptoms were severe and less often as the symptoms resolved. The patients were evaluated one year after the onset of the pain and again at the latest follow-up visit. Muscle strength was tested by means of a manual assessment of maximum strength and was graded subjectively by the senior one of us. No devices were used to measure strength at any of the follow-up examinations.
The intense pain continued for three to twenty-one days before spontaneous improvement was noted. As the intense pain subsided, it was replaced by a dull ache. Two patients noted a slight increase in the ache during use of the upper extremity for daily activities; the other five reported that the ache was constant and was not related to activity. No patient had persistent pain at night after the resolution of the initial intense pain. All patients noted the onset of weakness after the resolution of the initial intense pain. The onset of the subjective weakness occurred at a mean of approximately four weeks (range, one to six weeks) after the initial onset of the pain. Electromyographic and nerve-conduction testing revealed involvement of only the peripheral nervous system in all patients. Six patients had predominant involvement of one nerve: the suprascapular nerve in three patients and the long thoracic nerve in the other three. One patient had widespread, marked involvement of the entire upper trunk; electromyography revealed involvement of the infraspinatus, deltoid, and biceps muscles. That patient also had evidence of abnormalities distally along the course of the median nerve and was the only patient in the present study who had pain and paresthesias distally in the extremity. The pattern of electromyographic changes was consistent in all seven patients. Electromyographic testing that was performed three to four weeks after the onset of the pain showed fibrillation potentials and positive waves. Testing that was done three to four months after the onset revealed polyphasic action potentials with increased duration and amplitude but with a reduction in the number of action potentials. Physical examination at the time of presentation revealed objective weakness in six of the seven patients. All three patients who had involvement of the suprascapular nerve had weakness of external rotation and noticeable atrophy of the infraspinatus muscle. None of these three patients had obvious atrophy of the supraspinatus muscle or any weakness in the ability to elevate the upper extremity, although electromyography showed that all of them had denervation of both the supraspinatus and the infraspinatus muscle. Two of the three patients who had involvement of the long thoracic nerve had scapular winging at the time of presentation. The third such patient was initially evaluated three weeks after the onset of pain, at which time the findings on physical examination were normal. Weakness developed two weeks later, and an examination at that time revealed scapular winging. The patient who had diffuse involvement of the brachial plexus had atrophy and weakness of both the deltoid and the infraspinatus muscle at the time of presentation, four weeks after the onset of symptoms. Although electromyography revealed denervation changes in the biceps muscle, there were no abnormalities of the biceps on physical examination. One patient noted symptoms on the contralateral side fourteen months after the onset of the initial symptoms. Another patient had electromyographic testing of the asymptomatic, left shoulder at the time of the initial evaluation of the symptomatic, right shoulder. Although denervation changes, fibrillation potentials, and positive waves were noted in the asymptomatic shoulder, no symptoms had developed and no clinical abnormalities were noted in that shoulder at the time of the most recent examination. The patients were followed for a mean of six years (range, three to ten years) after the onset of the symptoms. All seven patients had a spontaneous decrease in pain during the follow-up period, and all reported the pain to be relatively minor within three months after its onset. At the one-year follow-up visit, six patients had no residual pain and one patient (the patient who had widespread involvement of the brachial plexus) had minor aching in the shoulder that occurred only after strenuous use of the extremity. At the latest follow-up visit, there was no difference, with regard to pain, for any patient as compared with the situation at the one-year follow-up evaluation. Although all patients reported subjective, gradual improvement of strength during the first year, manual testing at one year revealed full strength in only two patients. Both of these patients had had involvement of the long thoracic nerve. The third patient who had had involvement of that nerve still had some evidence of scapular winging, although it was less apparent than it had been at the time of the initial evaluation. All three patients who had had involvement of the suprascapular nerve, and the one who had had widespread neuropathy of the brachial plexus, had persistent weakness of external rotation at one year; however, the weakness was less severe than it had been at the initial evaluation. Some of the patients had additional improvement in strength between the one-year and latest follow-up visits. Manual muscle-testing revealed that four of the seven patients had normal strength; subjectively, all four thought that they had regained full strength. This group included the two patients who had had involvement of the long thoracic nerve and had recovered full strength at one year and two patients who had had involvement of the suprascapular nerve. The other three patients had nearly full strength but still noted slight weakness in the involved shoulder. Moderate weakness of external rotation remained in one patient who had had involvement of the suprascapular nerve and in the patient who had had widespread involvement of the brachial plexus. In addition, there was slight scapular winging in one patient who had had involvement of the long thoracic nerve, as stated previously.
The exact etiology of Parsonage-Turner syndrome has not been delineated, but both viral infection and immunological causes have been proposed6,7. In previously reported series, many patients were noted to have had an antecedent illness or a recent immunization3,5,8,9. Such an association could not be determined for any patient in the current series. Trauma generally is not considered to be a factor in the development of Parsonage-Turner syndrome1,8. Patients who had a history of trauma were included in the study by Mulvey et al., but there had been a prolonged asymptomatic period before the onset of pain. In addition, the injuries in those patients were very minor. One patient in the current series recalled that he may have sustained a minor injury of the affected shoulder before the onset of pain, but he had been asymptomatic for more than two weeks before the onset of symptoms. The age-range of the patients in our study was quite wide. A similarly wide range of ages has been reported in previous studies3,5,9,11. This syndrome typically has a large male-to-female ratio. All seven of our patients were male. Magee and DeJong reported a male-to-female ratio of 11.5 to one. Tsairis et al. and Turner and Parsonage11 found a much lower male-to-female ratio of two to one. A wide distribution of nerve involvement has been reported in the literature. In the original description by Parsonage and Turner5, the long thoracic nerve was involved most commonly; the suprascapular and axillary nerves were involved only if multiple peripheral-nerve lesions were found. Magee and DeJong as well as Tsairis et al. reported a much higher frequency of isolated involvement of the suprascapular nerve. Three of our seven patients in the present study had primary involvement of the suprascapular nerve as confirmed with both physical examination and electromyographic studies. Mulvey et al. reported on sixteen patients who had acute brachial neuritis with primary involvement of the phrenic nerve. No patient in the present study had involvement of the phrenic nerve. Previous authors have noted frequent bilateral involvement3,4,10, and it has been suggested9 that as many as one-third of patients have bilateral symptoms. Turner10 described the case of a patient in whom symptoms developed on the contralateral side approximately six months after the onset of the initial symptoms. In the current series, two of the seven patients had evidence of brachial neuritis on the contralateral side. Sensory changes frequently are noted in patients who have Parsonage-Turner syndrome. Tsairis et al. noted such changes in sixty-six (67 per cent) of ninety-nine patients who had this disorder. Turner10 noted no sensory changes in any patient in whom involvement was limited to a motor nerve with no cutaneous innervation. Six of the seven patients in the current series had primary involvement of either the long thoracic or the suprascapular nerve, both of which lack a cutaneous innervation. The one patient who had more widespread involvement of the brachial plexus had sensory changes in the hand, in the area of the median nerve. All seven patients had an increase in strength during the follow-up period, but only four stated that they had regained full strength. As reported by Dillin et al., most patients note an improvement in strength within the first two months after the onset of weakness. However, Magee and DeJong found that it may take as long as eight years to achieve maximum recovery. Patients with Parsonage-Turner syndrome who are seen soon after the onset of symptoms can pose a diagnostic challenge. This disorder can be confused with a variety of other diagnoses, including cervical radiculopathy, a tumor of the spinal cord, peripheral-nerve compression, amyotrophic lateral sclerosis, acute poliomyelitis, and abnormalities of the rotator cuff. The sudden onset of intense pain, with no inciting trauma and with normal findings on examination of the neck and shoulder, distinguishes this disorder from most of those included in the differential diagnosis. The diagnosis becomes more obvious when the pain decreases spontaneously and weakness develops. Electromyography at that time should confirm the neuropathy. The most confusing differential diagnosis is that of peripheral-nerve compression. However, patients who have that condition do not have the sudden, intense pain associated with Parsonage-Turner syndrome but rather have a more insidious onset of pain. Also, the fairly rapid, spontaneous resolution of pain that is typical in patients who have Parsonage-Turner syndrome is not seen in patients who have peripheral-nerve compression. During the period of the present study, thirteen patients had a diagnosis of isolated peripheral neuropathy of the shoulder that did not fit the pattern of Parsonage-Turner syndrome. Eight of these patients had an insidious onset of symptoms rather than the sudden onset of severe pain associated with acute brachial neuritis. All eight patients had weakness rather than pain as the primary symptom. Seven of these patients had involvement of the suprascapular nerve and one, the long thoracic nerve. Four patients who had involvement of the suprascapular nerve were found to have a ganglion cyst that was compressing the suprascapular nerve in the supraspinatus fossa. These ganglia were identified with use of magnetic resonance imaging. Five other patients had had a traumatic episode involving the shoulder that was suspected as being a factor in the etiology of the neuropathy. Three of these patients had involvement of the long thoracic nerve and two, the suprascapular nerve. None of these patients had sudden, intense pain after the initial trauma but rather an insidious onset of simultaneous weakness and mild pain. Although Parsonage-Turner syndrome is not seen frequently in a typical orthopaedic practice, it is still important for orthopaedists to be familiar with this disorder and to include it in the differential diagnosis when a patient describes pain or weakness about the shoulder. The diagnosis is made primarily by exclusion. The prognosis is reasonably good in that the pain typically resolves spontaneously. However, complete restoration of strength is not always achieved. Non-operative treatment is the accepted protocol, although recovery from this disorder can be quite protracted.
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.
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