Introduction 

Parsonage-Turner syndrome (PTS), an acute neurological disorder marked by shoulder pain, weakness, atrophy, and numbness, may also be termed neuralgic amyotrophy or idiopathic brachial plexopathy.¹ This disease affects individuals assigned male at birth (AMAB)at least twice as often as it affects individuals assigned female at birth (AFAB), primarily between the third and seventh decades of life.²

In some cases, the onset of PTS may occur after viral illnesses, vaccines, surgical procedures, or possibly even intense exercise, but the reason remains mostly unknown. 

As with other neurological or musculoskeletal diseases, there may be some misdiagnosis in PTS, resulting in some delays in receiving treatment. Being aware of the clinical features of PTS is required for diagnosing and treating this condition.

This article will examine the central clinical features of PTS: pain, weakness, and muscle wasting. By highlighting a clinical feature, we are hopeful that it will raise awareness in the healthcare community and strengthen the call for improved detection and intervention for this challenging diagnosis.

Overview of Parsonage-Turner Syndrome 

Aetiology and risk factors

• Infection (bacterial, viral, fungal)
• Surgery
• Rheumatic Disorder
• Connective tissue disorders such as Ehlers-Danlos Syndrome
• Systemic lupus erythematosus(SLE)
• Temporal arteritis
• Immunisations 
• Tetanus toxoid and antitoxin
• Diphtheria, pertussis, and tetanus (DPT) vaccine

Pathophysiology

While the precise mechanisms of PTS remain unclear, the primary hypothesis posits that it involves an inflammatory immune response of the brachial plexus and peripheral nerves. Inflammatory infiltrates and complement activation result in: 

• Axonal injury and demyelination of affected nerves
• Ischemia caused by inflammatory damage to the vasa nervorum
• Immune-mediated assault on nervous structures that is initiated by molecular mimicry following infection, vaccination, or surgical stress

Clinical spectrum of symptoms 

Parsonage-Turner Syndrome (PTS) usually develops in a predictable progression. Its onset is sudden and presents with severe, unilateral shoulder or upper arm pain, often described as burning or stabbing, which persists for days or weeks. After this episode of pain, patients develop weakness and/or paralysis of the arm when the shoulder girdle and upper arm muscles are affected. Progressive atrophy (muscle wasting) also develops in the following weeks and months as a result of denervation.⁴

Pain in Parsonage-Turner Syndrome 

Onset and nature of pain

The defining feature of Parsonage-Turner Syndrome (PTS) and often the first clinical symptom is pain. The pain generally starts suddenly, is severe, and commonly occurs during sleep.⁴

The pain is received as sharp, burning, stabbing, or throbbing in nature, characterising the acute inflammatory insult of the brachial plexus. Often, patients will report that the pain severity does not correlate with the severity seen in other musculoskeletal diagnoses, which may be a distinguishing feature of the syndrome.

Location

The shoulder and upper arm are the most typical sites of pain, while it may also extend into the neck, scapula, or forearm. Most cases present as unilateral involvement, but in rare cases, bilateral involvement has been recorded.⁴

Duration

The length of the painful period usually lasts anywhere from a few days to several weeks, and then lessens into the more disabling phase of muscle weakness and atrophy. Pain almost always has a preceding role before weakness, which is a clinical cue for early suspicion and diagnosis.

Impact on daily life

The impact of the significant acute pain phase on daily life is substantial. Sleep is often disrupted due to increased symptoms at night, and everyday tasks such as lifting, carrying, and overhead activities may be limited. Patients frequently experience functional disability that can result in distress and impact quality of life.

Differential diagnosis

Since pain predominates the early presentation, the differential diagnosis is broad and will include more common conditions such as rotator cuff injury, cervical radiculopathy, and adhesive capsulitis.

Clinical importance

This means detecting pain in the shoulder with associated weakness is very important clinically, since it is the first diagnostic indicator of PTS. Observing this pattern early in clinical practice provides a means for clinicians to distinguish between PTS and orthopaedic or spinal pathology and provide timely and appropriate diagnosis and management.

Weakness in Parsonage-Turner Syndrome 

Onset

Weakness is not present during the initial stage. Typically, weakness appears after pain subsides within 1-2 weeks. In some patients, weakness may appear more gradually, but the hallmark of the disorder is pain first followed by weakness.⁴

Pattern of weakness

In the PTS, the pattern of weakness is patchy. Its distribution depends on the nerves affected. Commonly involved nerves are the suprascapular, long thoracic, axillary, and anterior interosseous nerves.⁴

• Suprascapular Nerve: leads to weakness in shoulder abduction and external rotation
• long thoracic Nerve: causes scapular winging
• Axillary Nerve: Impairing deltoid strength
• Anterior Interosseous Nerve: producing deficits in thumb flexion and index finger flexion 

Functional impairments

Above all, disability causes functional impairment:

• Difficulty lifting the arm above the head
• Inability to rotate the shoulder
• Weak grip if the forearm muscles are involved

Neurological examination findings

On neurological examination, findings are that there is decreased power in specific muscles in specific nerve distributions. In some cases, it shows no sensory deficit.

Clinical importance

The clinical implications of weakness in PTS have both diagnostic and prognostic implications. In prompting a future EMG and/or nerve conduction study, the weak muscle groups will assist in localising the lesion to either the brachial plexus or its branches. As expected, the eventual study will validate a suspicion of axonal neuropathy. 

It is also the sequence of pain followed by patchy weakness with no significant sensory loss that is important in distinguishing PTS from cervical radiculopathy (without C4 or 5 sensory loss), rotator cuff tears, or peripheral nerve entrapment. 

In conclusion, weakness not only defines the disabling phase of PTS but also places you on a pathway toward the description and identification of a true diagnosis, therefore improving management.

Muscle wasting (atrophy) in Parsonage-Turner Syndrome 

Timeline

In Parsonage-Turner Syndrome, muscle wasting, or atrophy, typically happens within a few weeks to a few months after weakness develops. Typically, around two months after the initial onset of weakness, especially in the muscles surrounding the shoulder girdle.⁵

Commonly affected muscles

• Deltoid
• Supraspinatus
• Infraspinatus
• Serratus Anterior 
• Biceps (less common)

Clinical appearance

The clinical appearance that is seen includes visible hollowing of the supraspinatus–infraspinatus fossa of the shoulder, and it is also asymmetric in the unaffected side.²

Impact

The impact of atrophy is given below:

• Chronic disability, if it's severe
• Cosmetic concerns for patients
• Disability for overhead tasks 
• External rotation and lifting difficulties

Reversibility

Although some patients regain function over time, recovery is often incomplete and prolonged. Follow-up MRIs demonstrate that while acute oedema and inflammation may stabilise, there is still a possibility of mild but persistent atrophy and fatty infiltration in the long term.⁶ Some patients were left with permanent atrophy.

Diagnostic value

In terms of diagnosis, muscle wasting is helpful in determining whether a condition is chronic or longstanding PTS. The presence of atrophy on MRI or on exam, particularly when seen with the typical time line of pain → weakness → atrophy, supports the diagnosis, especially distinguishing it from more acute processes.

Associated clinical findings 

Parsonage-Turner Syndrome (PTS) is essentially a pain, weakness, and muscle-wasting condition, but other associated features may be present.

• Sensory disturbances in the form of numbness or paresthesia are seen in a small number of patients, suggesting limited sensory fibre involvement⁷
• Reflex changes can occur, which may include absent biceps, triceps, or brachioradialis reflexes in muscles that exhibit denervation⁸
• Bilateral involvement is rare in sporadic PTS; it can occur in recurrent or hereditary PTS. In some studies, bilateral symptoms were reported in 20% of patients⁹

Diagnostic Approach Based on Clinical Presentation 

• Clinical suspicion follows the triad: pain → weakness → wasting
• Important Role of a detailed history and physical exam
• EMG and nerve conduction studies can confirm denervation
• MRI can rule out other pathologies (i.e., cervical disc, rotator cuff tear)

Differential Diagnosis 

• Cervical radiculopathy: The most common mimicker of PTS is cervical radiculopathy, but cervical radiculopathy is classically associated with neck pain radiating in a dermatomal pattern with sensory changes, such as impaired sensation to pinprick and temperature. In contrast, PTS patients often have patchy weakness and minimal sensory changes
• Rotator cuff pathology and Adhesive capsulitis: Rotator cuff pathology and adhesive capsulitis may also demonstrate shoulder pain and range of motion abnormalities, but these particular causes do not display significant weakness and muscle wasting that occurs after PTS surgical treatment
• Motor neuron disease: Motor neuron diseases, most notably amyotrophic lateral sclerosis (ALS), may demonstrate progressive weakness and atrophy across multiple body parts. Normally, other atypicals present most of the time, typically bilaterally, progressively, and, most of the time, not associated with acute pain
• Peripheral nerve entrapment: The focal weakness of peripheral nerve entrapments (e.g., suprascapular or axillary nerve compression) will often mimic PTS, but they will generally present without an acute painful onset
• Myopathies: Myopathies will demonstrate proximal muscle weakness and atrophy like PTS, but these will often present bilaterally, and their elevated creatine kinase level will also separate them as different

Summary 

Parsonage-Turner Syndrome (PTS) is characterised by the sudden onset of pain and weakness followed by muscle atrophy. The hallmark difference between PTS, cervical radiculopathy, and rotator cuff pathology is the sequence in which one experiences pain, then weakness, and diminished motor function. PTS is diagnosed mainly by history, presenting symptoms, nerve studies, and EMG, which demonstrates evidence of nerve injury. An MRI is useful to help rule out other contributing factors of weakness, atrophy, and pain.

Management includes pain management, physical therapy, and longer-term follow-up. Although some people will go on to have persistent weakness or atrophy, most people will go on to make a full functional recovery. Being able to recognise PTS early is important to avoid misdiagnosis and unnecessary treatment.