Partial but rapid recovery from paralysis after immunomodulation during early stage of neuralgic amyotrophy.

[Medical Research Council (MRC) 2–3] was detected in the triceps brachii, f lexor carpi ulnaris and median nerve-innervated hand muscles. The flexor carpi radialis and ulnaris, extensor carpi ulnaris and finger flexors were mildly impaired. The shoulder girdle muscles, the biceps brachii, brachioradialis and extensor carpi radialis were spared. The muscle stretch reflexes were normal, except for a diminished left triceps jerk. There was no sensory deficit in the left upper limb. The routine blood test results were normal. The negative results included antiganglioside IgG and IgM antibodies, antinuclear antibodies, antineutrophil cytoplasmic antibodies, HBs antigens and serum Mproteins. Cerebrospinal fluid examination showed a normal cell count and protein content. A 3-day course of intravenous methylprednisolone (20 mg/kg daily) was prescribed, but there were no changes the next day. The patient underwent a 5day intravenous immunoglobulin course (0.4 g/kg daily) from days 7 through 11. Motor strength gradually returned during the regimen. On day 12 he could hold, pick up and release objects with his left hand, which had been useless before treatment. Although moderate left shoulder pain persisted, he went back to work on day 15. On follow-up examinations on day 54 his moDear Sir, Neuralgic amyotrophy is a well-established clinical syndrome characterized by an acute onset of shoulder and arm pain followed by muscular weakness, wasting and variable sensory loss [1] . Most neurophysiological studies have reported features of axonal degeneration [2] , reflecting terminal pathological results rather than the underlying process. We report a patient with neuralgic amyotrophy who was examined within a week after pain onset. The investigative results suggested that, in addition to axonal injury, reversible dysfunction within the brachial plexus played a part in the acute profound weakness.