Neuralgic amyotrophy: a clinical and electromyographic study.

The clinical syndrome of neuralgic amyotrophy is strikingly stereotyped. It consists of severe burning pain of sudden onset fn the outer aspect of the arm accompanied by wasting and weakness of the muscles of the upper limb. Affected muscles may be completely paralysed. The pain is occasionally transient, but usually lasts up to six weeks, and sometimes even longer. Weakness or paralysis follows its onset in the space of one to four days in 80% of cases. The motor symptoms are usually maximal at the outset, but progression over a period of seven days may be observed. The site of the pain and the muscles affected are not necessarily correlated. Paralysed muscles are flaccid and waste rapidly, but fasciculation is not obtrusive. Sensory changes occur most commonly when the circumflex nerve is affected. In the majority of patients sys temic disturbances?for example, malaise, fever?are minimal (Turner, 1944 ; Parsonage and Turner, 1948). Muscles affected are usually serratus anterior (Richardson, 1942), spinati, deltoid, and trapezius (Spillane, 1943), but any muscle of the arm may be deranged and bilateral involvement is quite common. Wyburn-Mason (1941) encountered 42 cases in a period of nine months, chiefly during the summer. Spillane (1943) described 46 cases in Service men, 26 of whom developed the disorder while they were in hospital for some other reason. Other authors have noticed a close association with hospital (Parsonage and Turner, 1948)* and French workers have often considered injections of serum?with brisk serum reactions?to be responsible (Pollet, 1924). This is not by any means an invariable experience (Richardson, 1942). Both sexes are affected ; in the earlier papers males preponderate in the ratio of 12:1, but Turner and Parsonage (1957) included nearly as many women as men. Age ranges of 30-79 (Wyburn Mason, 1941) and 16-54 years (Turner, 1944) have been quoted. Prognosis has been said to be poor where there is much muscle-wasting (Spillane, 1943 ; Turner, 1944), but Dixon and Dick (1945) described recovery taking up to two years in 13 out of 16 patients who had been severely affected. Turner and Parsonage (1957) agreed that return of power was the rule, the time needed for recovery varying with the nerves affected. Recurrent attacks have been described (Dixon and Dick, 1945). The site of the lesion responsible for the disorder has been variously suggested as the anterior primary rami of lower cervical and upper thoracic roots (Wyburn-Mason, 1941), with trunks of peripheral nerves affected in addition to or in isolation from the roots (Turner, 1944) and sometimes the spinal cord itself (Parsonage and Turner, 1948). No specific evidence for these conclusions has been offered. Necropsy evidence is lacking. The cause of the neuronal damage has been thought to be an inflammatory reaction of infectious or allergic origin. Electromyography may give some information regarding the site if not the aetiology of the lesion, and a group of patients with neuralgic amyotrophy have been examined in this way.