presentation suggested a bilateral C-5 radiculopathy. EMG studies revealed that this clinical picture was, in fact, produced by injury at the level of the brachial plexus, with a C-5, C-6, and C-7 denervation, and the authors proposed an ischemic mechanism that could involve the subclavian and axillary arteries.Typical pathologic findings of GCA occur in these vessel^.^ In our patient, however, only C-5 abnormalities were present in electrodiagnostic studies.Even if the ischemic mechanism remains unclear, the ipsilat-era1 vertebral artery was grossly abnormal in this patient, and the clinical response to corticosteroid therapy with concomitant improvement of the lumen of the vertebral artery on MRI angiography supports a local vascular mechanism caused by GCA.In conclusion, C-5 radiculopathy is a rare manifestation of GCA. After exclusion of radicular compression, the presence of other typical manifestations of GCA and, probably, angiographic abnormalities of the ipsilateral vertebral artery would be necessary for the diagnosis. The prognosis appears excellent with corticosteroid therapy.

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