Diagnosis
How is Parsonage Turner Syndrome Diagnosed?
Parsonage-Turner Syndrome is diagnosed predominately from the history and depending on the timing of the condition the physical examination can also give possible clues. Investigations are most often unhelpful but may be useful when other conditions in the differential diagnosis are possible.
History
Key Points for the History
- Severity of the pain
- Course of the illness
- a history of preceding events such as infection, immunization, strenuous exercise, trauma, surgery.
Diagnosis is predominately clinically based on the classical sequence of events:
- Sudden onset of severe pain (NRS of at least 7/10)
- Pain affecting the shoulder and / or arm
- Pain can last for at least a couple of weeks before giving way to muscular weakness.
- Muscular atrophy noticed in the affected muscles.
Diagnostic criteria [van Alfen 20061]
- Subacute or acute onset.
- Initial pain equal or greater than 7/10 for days or weeks.
- Multifocal distribution on the upper trunk, long thoracic nerve and suprascapular nerve.
- No obvious explanation for the neurological deficit.
Physical Examination
Examination maybe normal in the acute pain phase but will help to confirm reduced range of mobility. Pain is not usually affected by motion or palpation.
Look:
Notice any lack of symmetry of the neck, shoulder, chest, back and arms.
Look for loss of shape / muscular atrophy of the deltoid, supraspinatus, infraspinatus, trapezius and pectoralis muscles.
Look for winging of the scapula – This can occur at rest, with forward flexion of the arm or when the patient is pushing away from a wall in front of them. The long thoracic nerve innervates the serratus anterior muscle and stabilizes the scapula against the chest wall. If affected, the scapula will protrude from the chest wall medially and may sit more lateral. Winging of the scapula can also occur is trapezius muscle is affected and may also cause the scapula to be a few cms lower if both trapezius and serratus muscle is affected.
If trapezius muscle atrophy occurs there maybe also shoulder drop due to the weight of the arm pulling down on the shoulder.
Feel:
Examine for sensory change over the shoulder and upper limb. They are self-reported in up to 70% patients but is fund in up to 80% of patients on clinical examination.1
Paraesthesia or hypoesthesia is most common affecting the deltoid area and lateral shoulder but also occurs in the medial forearm and hand. Paraesthesia usually occurred at the onset of an attack or afterwards with traction on the affected parts of the plexus.
Move:
External Shoulder rotators – (posterior deltoid, infraspinatus, and teres minor muscles)
Patient holding arms close to the body flexed at 90o. Assess for strength of external rotation.
Serratus anterior –
Patient placing hand (side to be tested) on their opposite shoulder across their chest.
The examiner then places a hand on the opposite scapula and asks the patient to resist as a posterior force is applied to the elbow. Weakness is present if there is asymmetric scapular winging when compared to the opposite side.
Elbow flexors – (Biceps brachii, Brachioradialis & Brachialis)
With the arm at 90o and the examiners hand on the forearm and the biceps assess the patients strength at keeping the arm flexed when the forearm is pushed down.
Anterior Interossesus nerve – (nerve branch of the median nerve. Innervates the flexor pollicis, flexor digitorum profundus & pronator quadratus muscles). If this nerve is affected together with shoulder girdle weakness without trauma this is pathognomic for PTS.
Assess by having the patient make an “OK” with their thumb and index finger and then trying to prevent the examiner from “breaking” the okay by pulling.
Examination for other shoulder pathology
Cervical Radiculopathy - Spurling’s test.
The neck is passively extended and then rotated and laterally deviated to the symptomatic side. A positive test is when the patient’s sensory symptoms are reproduced with axial compression.
Musculoskeletal pathology
B) Palpation of the shoulder is a very easy way to assess for if one knows the surface anatomy.
Rotator cuff syndrome (tendonopathy or tendon tear) with pain at the insertion of the supraspinatus, Acromioclavicular joint pathology such as arthritis, and bicipital tendon pathology.
Rotator cuff impingement due to tendon pathology
Neer’s sign the examiner performs passive internal rotation of the arm.
Hawkin’s sign the examiner performs passive abduction and internal rotation of the arm. A positive sign is when there is shoulder pain with the movement.
Investigations
Laboratory investigations can normally show positive findings in 25% of patients but these findings often do not contribute directly to the diagnosis. In typical cases these are unnecessary.
Blood tests
Raised liver enzymes maybe seen as an association with Hepatitis E infection has been found in 10% of patients.2
Anti-ganglioside antibodies found in 26%
Lumbar puncture
CSF abnormal in 12.5% of cases tested. Abnormalities include elevated protein, slight pleocytosis and oligoclonal bands.
Electrodiagnostic tests
A common diagnostic test that is abnormal in 96% cases
Imaging Studies
Chest x-ray: useful to recognise a raised hemidiaphragm when phrenic neuropathy is also present.
Exclusion of a Pancoast (upper apical) lung tumour that may cause compression on the brachial plexus (usually the lower cord).
MRI cervical spine and shoulder:3
· Often not helpful to explain the clinical picture
· Can help to exclude other shoulder pathologies such as rotator cuff tear and impingement syndrome.
· Can help to exclude cervical radiculopathies caused by cervical disc herniation (but asymptomatic disc herniation possible).
· Denervation oedema of the affected muscle can be seen at an early stage.
Ultrasound (research based)4
· Increased cross sectional area of affected nerves compared to non-affected sides and control volunteers.
· Constrictions have been found at single or multiple points along an effected nerve or nerve fascicle. The constrictions are always bordered by swelling and maybe incomplete or complete.5
References
1. Nens van Alfen & Baziel G. M. van Engelen. The clinical spectrum of neuralgic amyotrophy in 246 cases, Brain, 2006, 129, 438–450. https://doi.org/10.1093/brain/awh722
2. van Eijk, Jeroen J J et al. “Neuralgic amyotrophy and hepatitis E virus infection.” Neurology vol. 82,6 (2014): 498-503. https://doi.org/10.1212/WNL.0000000000000112
3. M. Ryan, A. Twair, E. Nelson, D. Brennan & S. Eustace (2004) Whole Body Magnetic Resonance Imaging in the Diagnosis of Parsonage Turner Syndrome, Acta Radiologica, 45:5, 534-539. https://doi.org/10.1080/02841850410006083
4. van Rosmalen, M., Lieba-Samal, D., Pillen, S. and van Alfen, N. (2019), Ultrasound of peripheral nerves in neuralgic amyotrophy. Muscle Nerve, 59: 55-59. https://doi.org/10.1002/mus.26322
5. ArÁnyi, Z., Csillik, A., DéVay, K., Rosero, M., Barsi, P., BÖhm, J. and Schelle, T. (2017), Ultrasonography in neuralgic amyotrophy: Sensitivity, spectrum of findings, and clinical correlations. Muscle Nerve, 56: 1054-1062. https://doi.org/10.1002/mus.25708