Intra-arterial nimodipine for the treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results

Abstract

Background and purpose: Cerebral vasospasm remains a major problem in patients recovering from aneurysmal subarachnoid hemorrhage despite advances in medical, surgical, and endovascular care. Our purpose was to assess the efficacy of intra-arterial nimodipine, a calcium-channel blocker acting mainly on cerebral vessels, in preventing delayed neurologic deficits in patients with symptomatic vasospasm.

Methods: Clinical charts of 25 consecutively treated patients were retrospectively reviewed. A multifactorial decision tree was used to determine the indication for angiography and subsequent endovascular treatment. Nimodipine was infused intra-arterially via a diagnostic catheter in the internal carotid artery or vertebral artery at a rate of 0.1 mg/min. Angiographic vasospasm before endovascular treatment, immediate vessel caliber modifications, and short- and long-term clinical efficacy of the procedure were assessed.

Results: Thirty procedures were performed in 25 patients. Clinical improvement was observed in 19 (76%), 16 of whom improved after the first endovascular procedure, two after the second intra-arterial treatment, and one after the third. Of these 19 patients, only 12 (63%) had notable vascular dilatation at postprocedural angiography. Dilatation of infused vessels occurred in only 13 (43%) of 30 procedures. After follow-up of 3-6 months, 18 (72%) of 25 patients had a favorable outcome (Glasgow outcome scale score of 1-2 and modified Rankin scale score of 0-2). No complications were observed.

Conclusion: Intra-arterial nimodipine is effective and safe for the treatment of symptomatic vasospasm after subarachnoid hemorrhage. Further prospective randomized studies of cerebral blood flow are needed to confirm these results.

Fig 1.

Case 25. This patient presented with a decreased level of consciousness and was treated with intra-arterial nimodipine for symptomatic cerebral vasospasm following SAH. A and B, Anteroposterior (A) and lateral (B) angiograms of the left internal carotid artery show vasospasm at the level of the carotid siphon, the terminal internal carotid artery, the A1 segment of the ACA, and the MCA. C and D, Anteroposterior (C) and lateral (D) angiograms obtained after intra-arterial injection of nimodipine 3 mg into the internal carotid artery demonstrate an increased diameter of the vessels. The patient’s clinical condition rapidly improved after treatment.

Fig 2.

Case 4. This patient with right hemiparesis was treated with intra-arterial nimodipine for symptomatic cerebral vasospasm following SAH. This patient had moderate vasospasm of tICA, ACA and MCA on the left side. A, Lateral angiogram of the left internal carotid artery shows vasospasm involving also the distal cerebral branches (arrows). B, Lateral angiogram of the left internal carotid artery obtained after the intra-arterial injection of nimodipine 2 mg shows a slight increase in the size of the distal arteries (arrows) and the internal carotid system. Despite the poor angiographic results, the patient’s condition improved significantly within 12 hours, and no recurrence of symptoms was observed.

Fig 3.

Case 12. Patient presenting with left hemiparesis and diffuse and severe vasospasm. After an intra-arterial injection of 3 mg of nimodipine into both carotid arteries and the basilar artery, angiographic and clinical results were poor. A second session with injection of 5 mg of nimodipine into the same vessels achieved good angiographic results and clinical improvement. A, This angiogram obtained before the intra-arterial injection of nimodipine shows a moderate vasospasm of the left vertebral artery. (Vasospasm was severe in the other vessels, not shown.) B, After nimodipine therapy, this left vertebral artery angiogram shows increased size of the basilar artery. Despite these results, the patient later died from cardiopulmonary complications.