Electroconvulsive Therapy and Venous Angiomas Two Case Reports and Review of the Literature Sohrab Zahedi, MD, Clifford Yang, MD, Donal O’Hanlon, MD, Kaloyan Tanev, MD, and William P. Shea, MD Abstract: According to the American Psychiatric Association, the risk for complications related to the electroconvulsive therapy (ECT) treatment of patients with cerebrovascular malformations is small. The literature contains a number of case studies presenting the uneventful treatment of patients with cerebral aneurysms with ECT. However, there is a paucity of cases presenting ECT in the context of a cerebral venous angioma. In this article, we present 2 cases of patients treated with ECT who were found to have documented venous angiomas. This is followed with a brief review of the literature. Key Words: ECT, electroconvulsive therapy, venous angioma (J ECT 2006;22:228Y230) I n 2001, the American Psychiatric Association Task Force on Electroconvulsive therapy (ECT) considered the risk of bleeding from cerebrovascular malformationsVaneurysms, arteriovenous malformations, and venous angiomasVin patients undergoing ECT to be small. 1 It also recommended the use of short-acting antihypertensive agents to blunt the hypertensive surge associated with the procedure. A number of case reports in the literature have reported the uneventful use of ECT on patients who were found to have a cerebral aneurysm; that is, no adverse events resulted from the vascular anomalies. Based on our research, there have been only 3 case reports documenting the use of ECT on patients with cerebral venous angiomas. Much like the case of cerebral aneurysms, it is generally agreed that with adequate intraprocedure con- trol of the blood pressure (BP), patients with cerebral venous angiomas can be safely treated with ECT. In this article, we present 2 patients with cerebral venous angiomas that were treated with ECT without any cerebral vascular com- plications. A brief review of the literature follows in the Discussion section. CASE REPORTS M.C. is a 42-year-old white divorced woman with a history of severe chronic major depressive disorder and posttraumatic stress disorder who had been treated with multiple antidepressants during a 7-year period. Her past medical history was significant for hyperten- sion, asthma, migraine headaches, and gastroesophageal reflux disease. Based on her long history of nonresponsiveness to a number of oral antidepressants including fluoxetine, escitalopram, sertraline, duloxetine, buproprion, quetiapine, and lithium, it was agreed that ECT would be attempted. Based on a pre-ECT magnetic resonance imaging (MRI) that was done for the evaluation of her history of migraine headaches, a left thalamic venous angioma was discovered (Fig. 1). In addition to an evaluation by the internal medicine team who cleared the patient for ECT, the neurosurgical team also evaluated her, and she was cleared for ECT with the recommendation to have her BP controlled during the procedure. Although unlikely, we could not at that time definitively say that the headaches were not related to the venous anomaly. After informed consent was obtained, M.C. underwent her first course of unilateral ECT treatment. Beta-blocking agents were used to control the intraprocedural rise in BP. The maximum BP recorded reached 191/111. The patient tolerated the procedures well and had a mild improvement in her depressive symptoms with a unilateral regimen that was then switched to a bifrontal ECT approach with good results. This led to the development of some reversible cognitive difficulties, which led us to interrupt the course. Because of the recurrence of severe depression, we later resumed unilateral ECT and she again seemed to have a mild response. Interestingly, her migraine headaches resolved during ECT and she has not had any clinical complications related to the venous angioma. The second course of ECT was terminated because of memory impairment as well. FIGURE 1. T1-weighted postcontrast axial image at the level of lateral ventricles shows 2-cm left thalamic venous (arrow). From the Departments of Psychiatry and Radiology, University of Connecti- cut Health Center, Farmington, CT. Received for publication May 23, 2006; accepted June 8, 2006. Reprints: William P. Shea, MD, Department of Psychiatry, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030 (e-mail: shea@psychiatry.uchc.edu). Copyright * 2006 by Lippincott Williams & Wilkins CASE REPORT 228 J ECT & Volume 22, Number 3, September 2006 Copyr ight © Lippincott Williams & Wilkins. Unauthor iz ed reproduction of this article is prohibited.