Sir Charles Bell first drew attention to the long thoracic nerve in 1821.¹ Lesions of the nerve cause winging of the scapula with medial transition of the scapula and prominence of the vertebral border.² Skillern in 1913 first observed that the nerve is exposed to trauma in the root of the neck. He wrote:

“The long thoracic nerve is exposed to trauma as it traverses the scalenius medius.”

The nerve itself is small in diameter and fragile and is vulnerable at many sites, particularly within the scalenus medius.³

The commonest long thoracic nerve lesion encountered by neurologists is acute brachial plexus neuropathy (neuralgic amyotrophy), which is less common than trauma, accounting for only 5–10% of all cases.⁴ In 1943, describing 46 patients with “localised neuritis of the shoulder girdle” Spillane⁵ gave the first full description, elegantly summarised in his renowned text:⁶

“There is acute onset of pain in the shoulder and side of the neck, over the scapula and down the affected arm usually not further than the elbow…The pain is commonly worse at night, disturbing or preventing sleep…and usually persists for a week or 10 days…little or no general upset, no stiffness of the neck and upper limb reflexes may remain unaltered. After a few days or when the pain is subsiding, paralysis supervenes. The muscles most commonly affected are the serratus, the spinati, the deltoid and the trapezii in that order. The neuritis may be bilateral…Sensory loss is as a rule slight or absent; a small zone of hypo-aesthesia over an affected deltoid muscle…The prognosis is good but affected muscles often waste rapidly and recovery is slow…a year or more. Rarely there may be a recurrence in the same or opposite shoulder.”

A year later Aldren Turner⁷ provided a similar account. The disorder is sometimes named after Parsonage and Turner,⁸ who provided further examples. In 66 of their original 136 patients, they found possible precipitating causes that included operations, infections, inoculations, and trauma to remote areas. Familial, post-infective (for example influenza, coxsackievirus, infectious mononucleosis, Borrelia burgdorferi) and post-vaccination factors have been described, but the aetiology is unknown in many examples. Meuleman et al suggested that Dreschfeld⁹ (1885) may have published the first report of hereditary neuralgic amyotrophy, that of a 43 year old woman who had suffered three episodes of painful upper limb weakness and whose sister had suffered seven similar attacks.

A possible earlier example was described as “spontaneous parenchymatous neuritis” in which Joffroy in 1879 showed loss of myelinated fibres.¹⁰