Brachial neuritis

A 33-year-old right-handed woman was admitted for rehabilitation with a history of sudden onset of acute pain in her right shoulder, August 2010. The pain was sharp, moderate to severe in intensity and lasted almost four days resulting in drooping and prominence of her shoulder joint. The residual impairment was weakness in her shoulder. As a result there was difficulty in performing activities of daily living and domestic chores with the right arm. 

She did not have a preceding history of any viral or bacterial infection nor had she received any form of vaccination pre-event. 

Examination and assessment

On admission, the scapula was in a constant “winged” position, at a 90 degree angle to the thoracic rib cage. It was abducted and laterally rotated. 

There was limited shoulder abduction and flexion, power was generally 3/5 with reduced reflexes and normal tone. 

There was no sensation to light touch or pinprick in digits, thumb distally or within the palm with impaired proprioception.

Investigations 

Electromyography (EMG) showed patchy, right upper brachial plexopathy of mild-to-moderate severity with some features of re-innervation. Her MRI of the shoulder and spine were normal. 

Diagnosis: brachial neuritis

Brachial neuritis is a relatively rare condition that describes inflammation of the brachial plexus manifesting as sudden-onset pain in the shoulder and the arm followed by weakness and/or numbness.

It is also known by a variety of names, eg:

• Parsonage-Aldren-Turner syndrome
• Brachial plexitis
• Brachial plexopathy
• Acute brachial radiculitis.¹

According to McCarty et al, so far there has been no substantial evidence supporting an aetiological mechanism for the pathogenesis of brachial neuritis.² However, a viral aetiology is the most emphasised aetiology with various infections preceding the onset of symptoms in about 25% of cases. Up to 15% of cases have been reported to occur following vaccinations. 

Other proposals include autoimmune mechanisms, surgery, heavy exertion and trauma. A hereditary association has also been reported.²

Despite the lack of evidence supporting the aetiology, the clinical presentation seems to be persistent and primarily based on two symptoms. The first symptom is sudden-onset pain in the shoulder and/or upper arm.² The pain is described as piercing, sharp and radiating. 

The pain subsides within few hours or two to three weeks.² As the pain diminishes, the second symptom, ie. muscle weakness affecting the arm and shoulder, sets in.² The arm becomes weak in multiple different muscles and can be profound. It can last for a few months or up to a year. 

Physical examination reveals abnormalities in the distribution of the brachial plexus with involvement of one or more nerves.

Sensory changes have been noted to be minimal in degree as compared to motor deficits. Sensory loss usually follows the distribution of the affected motor nerves.²

Patients with Parsonage-Turner syndrome at the time of onset of symptoms can present as a diagnostic challenge. It can be confused with a wide list of differential diagnoses, including cervical radiculopathy, peripheral nerve compression, amyotrophic lateral sclerosis, acute poliomyelitis, tumour of the spinal cord and abnormalities of the rotator cuff.³

An accurate diagnosis in this condition is imperative. A compressive lesion such as a cervical herniated disc needs to be ruled out by an MRI cervical spine scan early on. An EMG study can be performed after three weeks to confirm the diagnosis.¹

EMG is the cornerstone of diagnosis as it differentiates brachial neuritis from traumatic upper trunk or plexus lesions. It is usually performed after three weeks of symptom onset. 

Findings depend upon the severity of neural damage and usually reveal fibrillation potentials and positive waves suggestive of muscle denervation. Delayed distal latencies and decreased amplitude of active potentials are also present.²

Treatment in the acute phase is focused on reducing the pain. Patient is advised rest or reduced activity, oral steroids to decrease the inflammation and use of narcotic medications if they are needed for pain control. Neurotropic medications like gabapentin and pregabalin can be started early on to stabilise the nerve membranes and limit the pain.¹

Once the pain has subsided, long-term management requires upper-extremity and upper-body rehabilitation to regain strength. Range of motion begins passively –change to active rehabilitation once the patient recovers some strength.² Non-operative treatment is the accepted protocol.³

Recovery is mostly good. Improvement in strength begins from after one month to three years.² McCarty et al and Tsaitis et al estimated complete recovery to be 89% after three years. 

The greater the severity and duration of the pain and weakness, the longer the recovery time.²

Management 

This patient underwent an intensive physiotherapy and occupational therapy intervention along with NSAIDs and neuropathic painkillers.

Physiotherapy

Before the strengthening of her shoulder muscles could begin, a lot of hands-on soft tissue work around her scapulae muscles had to be done to release the tight muscles that were keeping her right scapula in an abducted and laterally rotated position.

She was provided a shoulder cuff. Initially she was started off with gravity-assisted exercises for the shoulder. Over the weeks, her strength began to increase in her shoulder muscles and she was able to start doing active range of movement exercises against gravity.  

As an adjunct to physiotherapy, electrodes were placed on two rotator cuff muscles or on her rhomboids and her levator scapulae to electrically stimulate the muscle to contract using a neuromuscular stimulator machine. This helped to strengthen the atrophied muscles.

Occupational therapy 

An occupational therapy programme was organised for her which focused on exploring optimum use of her right upper limb in functional activity. 

Education included supporting elbow/hand for table top activities and use of compensatory tools such as buttering and spike boards in meal preparation. The programme also incorporated activities which work on increasing grip strength and dexterity. 

For sensory deficits, she was engaged in a sensory re-education programme and was educated regarding the use of vision to compensate for sensory deficits. Other interventions included exploring vocational options, housing, return to driving and re-engagement in family and community roles. 

Three months after discharge, she was independent in all daily activities.

References

1. Ullrich PF. Brachial neuritis treatment and prognosis 1999 [http://www.spine-health.com/conditions/neck-pain/brachial-neuritis-treatment-and-prognosis]
2. Hosey RG, Rodenberg RE. Brachial neuritis: an uncommon cause of shoulder pain. Orthopedics 2004; 27(8): 833-6
3. Misamore GW, Lehman DE. Parsonage-Turner syndrome (acute brachial neuritis). J Bone Joint Surg Am 1996; 78(9): 1405-1408