Steroids are empirically used to medicate patients with myelopathy of unknown etiology. We report the reversible aggravation of neurological status after steroid administration in a patient with venous congestive myelopathy (VCM). We retrospectively evaluated 36 patients with angio-graphically confirmed spinal arteriovenous malformation (SAVM) from a prospectively collected neurointerventional database. We evaluated steroid medication and neurological aggravation using Aminoff grading and analyzed using Fisher's exact test whether steroid medication is related to neurological aggravation and spinal cord edema as demonstrated on MR T2-WI. Among 26 patients who had been treated with steroids, ten had aggravated neurological deficits. The aggravation in these ten patients was related to the steroid medication (P = 0.039 in all patients) and only marginally to VCM with spinal cord edema as seen on T2-WI (P = 0.074). Aggravation caused by using a high intravenous dose (250–1000 mg) of methylprednisolone or dexamethasone at 8–20 mg/day slowly decreased after stopping the steroid medication. Steroids were reversibly detrimental in patients with VCM caused by SAVM. A history of neurological aggravation after the use of steroids may suggest the diagnosis of SAVM associated with VCM.

We report our experience with endovascular treatment of supra-aortic arteries and follow-up results in patients with Takayasu's arteritis (TA) presenting with neurological symptoms. Of the 20 patients with TA who underwent cerebral angiography for neurological manifestations between May 2002 and May 2009, 12 (11 females, one male; mean age, 39 years; range 31–56 years) underwent endovascular treatment and evaluated outcome for 21 lesions, including nine common carotid arteries, four vertebral arteries, four subclavian arteries, two internal carotid arteries, and one brachiocephalic artery. Eight patients underwent multiple endovascular procedures for different lesions in single or multiple stages. Mean angiographic and clinical follow-up durations were 34 months (range, 11–79 months) and 39 months (range 11–91 months), respectively. Technical success was achieved for 20 procedures in 11 patients. One procedure failed, with 50% residual stenosis after stenting due to dense calcification of vessel walls. There were no procedure-related complications. Restenosis occurred at two lesions in two patients were treated by re-stenting. Asymptomatic occlusion occurred at two lesions in one patient. Ten patients remained in 0–1 on the modified Rankin scale (mRs) during mean 39 months. One patient, however, had a score of 3 on mRs due to a traumatic contusion during follow-up. One patient died from cardiac failure 36 months after successful angioplasty. Our data suggest that endovascular treatment of symptomatic supra-aortic lesions of TA is effective and durable in selected patients with neurologic symptoms.

Aggravating headache accompanied by nausea and epigastric discomfort suggesting a warning leak in a 39-year-old woman with a giant thrombosed intracranial aneurysm prompted us to undertake coiling of the aneurysm. After uneventful coil embolization of the aneurysm, collapse of the lung related to bronchospam developed, and was found to have a gastrointestinal pathology which had gone undetected before the procedure. Despite its rarity, gastrointestinal pathology mimicking warning leak should have been considered in a patient with a warning leak sign.