Parsonage-Turner Syndrome

                                   Dr. KS Dhillon

Introduction

Parsonage-Turner Syndrome (PTS) is also known as neuralgic amyotrophy or brachial neuritis. It is a rare syndrome that can occur in normal healthy individuals. It presents with sudden onset of unilateral shoulder pain that quickly amplifies in severity and intensity. The acute period of pain is replaced over the next few days to weeks with progressive weakness, reflex changes, and sensory abnormalities in the shoulder girdle and proximal upper limb muscles. The condition has been reported in numerous clinical situations that involve some sort of antecedent impact on the patient, whether it be surgical, traumatic, infectious, or even therapeutic, such as cases involving antibiotic treatment or vaccinations. The suprascapular and axillary nerves and their corresponding muscles are affected most frequently. PTS is frequently misdiagnosed and is often under-recognized. A delay in the diagnosis of PTS results in continuous severe pain and a reduction in activities of daily living for patients. Although PTS is a rare disease, prompt diagnosis and effective therapeutic interventions are very important.

Diagnosis is made clinically with a neurological examination that may find moderate motor-sensory changes to flaccid paralysis of the upper extremity. Nerve conduction and EMG studies can confirm the clinical findings. Treatment is by observation and pain control. Recovery can take upto 3 years. Operative nerve exploration, neurolysis, nerve transfer, or tendon transfer may be needed in patients if there is no evidence of EMG recovery by 9-12 months.

Overview, etiology, and incidence

Idiopathic brachial plexopathy was first reported by Parsonage and Turner in 1948 [1]. The condition had previously been described in the literature as far back as 1897 prior to the extensive study of the syndrome by Parsonage and Turner [2-6].

PTS is a condition in which the patient suddenly develops severe unilateral shoulder girdle pain [1]. This pain can extend to the trapezius ridge, upper arm, forearm, and hand [7]. The pain is usually worse at night and may awaken the patient from sleep. Usually, there are no constitutional symptoms [1,8,9]. The pain is almost always self-limiting. It lasts for 1 to 2 weeks, but on rare occasions persists for longer periods [10-12]. 

Weakness usually develops a few days to weeks after the initial onset of pain. The prevalence of sensory deficits varies. One study reported sensory deficit in 66% of patients [13] while another study found sensory deficit in a minority of patients [14]. 

Weakness may not be recognized immediately because of the inability to test muscle strength due to the debilitating pain. Weakness may also not be detected if it involves muscles that are difficult to test, such as the serratus anterior or the supraspinatus muscle. Within a month, the weakness is usually obvious and muscle wasting becomes obvious. Scapular winging is seen in patients who have involvement of the scapulothoracic nerve that innervates the serratus anterior muscle. 

The diagnosis of PTS can sometimes be elusive and the treatment can be delayed. PTS is a diagnosis that should always be entertained in any patient who presents with acute shoulder girdle pain.

The pathophysiologic events that cause PTS have not been fully elucidated but various risk factors and antecedent events have been identified in 28–83% of the patients [8,15,16,17,18,19,20]. Some of the etiological associations found with Parsonage-Turner Syndrome include:

1. Infection

•  Bacterial

•  Parasitic

•  Viral

2. Surgery

3. Anesthesia

4. Hereditary 

• Rheumatic disease

5. Connective tissue disorders (i.e., Ehlers-Danlos Syndrome)

•  Systemic lupus erythematosus

•  Temporal arteritis 

•  Polyarteritis nodosa

6. Trauma

•  Remote from the shoulder girdle

7. Stressful exercise

8. Smallpox

9. Tetanus toxoid and antitoxin

10. Diphtheria, pertussis, tetanus (DPT) vaccine

11. Immunizations

12. Swine flu

13. Pregnancy and childbirth

14. Radiation therapy

15. Lumbar puncture

16. Pneumoencephalogram

17. Radiologic contrast dye administration

18. Allergy desensitization

There are several risk factors associated with the development of PTS. The most common is a recent viral illness. One study showed that 25% of patients had a recent viral illness before the appearance of PTS symptoms [21]. Recent immunization is the second most common risk factor. About 15% of individuals who developed PTS have a recent history of immunization [21]. The most common cases of PTS are attributed to either a viral illness directly involving the brachial plexus or an autoimmune response to the viral infection or to the viral antigen in the immunization. There is an association between certain diseases and the pathophysiologic development of PTS. Systemic lupus erythematous, temporal arteritis, and polyarteritis nodosa all have a vasculitic component, hence, a vascular etiology is proposed as a cause of PTS in these conditions. The symptoms of pain of PTS are believed to be due to ischemia. Ischemia, whether it is inflammatory or mechanical in nature, may be one explanation for the sudden onset of severe pain. Nerve biopsies have shown evidence of ischemic changes in the form of perineural thickening, neovascularization, and focal fiber loss in PTS. The ischemic changes are believed to have an immune pathogenesis [22].

The overall reported incidence of PTS is 1.64 cases per 100,000 people [23]. The true incidence may be higher due to underreporting because of difficulty in making the appropriate diagnosis. 

Overall, there is a higher incidence in men than in women. The age range is from 3 months of age [12] to 75 years [24]. The highest incidence of PTS occurs in individuals between the third and seventh decades [12].

PTS association with surgical procedures

Parsonage-Turner Syndrome’s association with surgical procedures has been extensively reported [17,25,26]. In these cases, PTS usually occurs in the postoperative period and, in some cases, during rehabilitation.

The surgeries include a variety of orthopedic procedures, hysteroscopy, coronary artery bypass surgery, and oral surgery [17,25,27,28,29,30,31, 32].

Several mechanisms have been postulated for the onset of PTS in such cases. There are two leading theories regarding the etiology of postsurgical PTS. These include traction injury to the brachial plexus due to improper patient positioning during surgery and immune-mediated inflammation of the brachial plexus. Inappropriate position, traction, or pressure injuries during operative procedures can cause PTS. Sternal traction during coronary artery bypass surgery has been postulated to result in brachial plexus compression. Injury to the plexus can also occur when the arms are over-abducted in a prone or supine position. There is mounting evidence that PTS also occurs in surgical procedures that involve little to no traction or compression injury to the brachial plexus [25,30,31].

PTS symptoms following surgery develop within 24 hrs of the procedure or may take up to a week or more following surgery. The differential diagnosis in patients presenting with severe, unilateral shoulder pain includes cervical disk herniations or foraminal stenosis causing cervical radiculopathy or mass lesions compressing the brachial plexus or individual nerves. 

Conditions such as postherpetic neuralgia, calcific tendonitis, acute subacromial bursitis, and adhesive capsulitis can also present with similar symptoms. Brachial plexopathies such as thoracic outlet syndrome can also present with less acute and severe pain [33,34,35,36,37]. 

In patients with postherpetic neuralgia, the classic skin lesion makes the diagnosis fairly obvious. Patients with shingles who present without rash,  the diagnosis can be more elusive [38]. 

Patients with cervical radiculopathy often have a positive Spurling maneuver [39]. This maneuver is negative in patients with PTS.

Symptoms due to calcific tendonitis or acute subacromial bursitis will be aggravated with shoulder motion, particularly impingement-like maneuvers. In such patients, cortisone injections or even a diagnostic lidocaine injection can provide immediate pain relief and that helps to establish a definitive diagnosis.

There are several similarities between PTS and adhesive capsulitis. Both present with severe pain, which is worse at night, and the pain is unremitting regardless of position. Both are idiopathic conditions that have a nonspecific inflammatory component. They will resolve spontaneously with a relatively good long-term prognosis for recovery of function [40,41]. There is, however, one major difference. Patients with PTS do not experience a significant loss of glenohumeral range of motion, unlike patients with adhesive capsulitis. Glenohumeral motion is usually completely preserved in PTS. 

PTS usually involves one upper limb, but bilateral involvement has been reported. In some cases, abnormal EMG changes can be identified in the contralateral asymptomatic limb. The upper trunk of the brachial plexus, the long thoracic nerve, the suprascapular nerve, and the axillary nerves are most commonly involved [8,39,42,43,44,45]. Involvement of the anterior interosseous, musculocutaneous, and spinal accessory nerves is less common [13,42,46,47]. The ulnar, radial, and median nerves are least commonly involved [1,12,48,49]. Rarely the middle and lower trunks can be involved [12]. Root-level involvement is rare and the paraspinal muscles are usually spared [50,51]. Involvement of the phrenic nerve has also been reported [52,53,54,55]. These patients present with shortness of breath and chest x-rays will show an elevated hemidiaphragm. 

There are reports of lumbosacral plexus involvement, but most of these patients have underlying medical illnesses and this suggests that there may be other contributing factors [56,57,58,59]. The lateral antebrachial cutaneous (LAC) sensory nerve is affected in about 32% of cases [60]. There is one unique and often diagnostic feature of PTS and that is the involvement may not follow a classic nerve or plexus pattern. One can see the involvement of the suprascapular and long thoracic nerves while sparing other nerves and muscles such as the deltoid and biceps that may share the same root or plexus level.

Electromyographic study 

The diagnosis of PTS is dependent on the EMG portion of the electrodiagnostic exam [61,62]. 

In the involved muscles, there is widespread denervation and often there is complete denervation. A thorough physical exam with extensive muscle testing is carried out before a complete EMG exam. PTS is an axonal disorder commonly affecting the proximal muscles of the upper limb, hence the motor and sensory nerve conduction velocities and distal latencies tested on the distal upper limb are usually normal. 

Since the LAC sensory nerve is commonly involved, testing of the LAC sensory nerve bilaterally for comparison should be carried out [60]. If there is a significant asymmetry i.e greater than 50% drop in the involved LAC sensory amplitude, testing of the superficial radial sensory amplitudes should be carried out to help rule out a brachial plexopathy from other causes, such as mass lesions in the supraclavicular fossa or other possible pathologies [61,64].

There are no large natural history studies on the recovery of PTS based on EMG findings. Reinnervation usually begins to occur somewhere between 6 months and 1 year. The axonal regeneration usually occurs at a rate of 1–4 mm/day. 

EMG is a form of diagnostic testing that can better identify, isolate, and grade the severity of denervation and, after a period of time, reinnervation of the involved muscles. 

Treatment

In the initial stage of the disease, the pain is managed with opiates, NSAIDs, and neuroleptics [43,65,66]. In addition to medications acupuncture and transcutaneous electrical nerve stimulation (TENS) can also be used.

Oral steroids have been used for the treatment of PTS, but there is poor evidence in the literature to support its efficacy [61]. Oral prednisone given in the first month after the onset of symptoms shortens the duration of symptoms according to one study. However, further studies are needed to establish the efficacy of treatment with corticosteroids or other immune-modulating therapies [67]. A recent study of postsurgical patients who developed peripheral neuropathies showed that immunotherapy produced meaningful improvement in neurological symptoms and impairments [68].

In patients presenting with a classic shingles rash or when postherpetic neuralgia is suspected antiviral medications should be considered [7,69,  70,71,72].

Physical therapy is useful for the treatment of PTS. Once the painful stage is over a more aggressive treatment plan can be instituted. Muscle strengthening exercises are started if there is muscle denervation and muscle weakness. Range of motion exercises are needed if there is joint limitation of movements.

Functional conditioning of the upper extremity can be useful in patients with brachial neuritis. Assistive devices and orthotics can be used, depending on the particular disabilities present.

In some patients, nerve grafting or tendon transfers may be necessary for the few patients who do not achieve good recovery by 2 years. Surgery is aimed at improving shoulder abduction. In some patients, neurolysis of the nerves may be required.

Conclusion

PTS usually appears suddenly and presents with disabling pain. It is usually difficult to diagnose in the acute state. The pain in this condition is usually self-limiting. The natural history of PTS leads to a favorable functional recovery.

Early diagnosis with clinical evaluation, electrodiagnostics, and relevant imaging can allow for early pain management. A proper diagnosis can also avoid unnecessary additional investigations or surgical intervention.  Follow-up EMG testing is useful for demonstrating early electrodiagnostic signs of recovery which can precede clinical evidence of recovery. This finding can provide the doctors with information regarding the patient's prognosis and, ultimately, recovery.

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