Endovascular treatment of cerebral vasospasm.

Abbreviations: ICP intracranial pressure, TCD transcranial Doppler sonography THE following scenario is very frustrating for all concerned. A patient presents with the “worst headache of my life.” Radiology is involved with the patient from the outset, including making the diagnosis of subarachnoid hemorrhage by computed tomography (CT) and the aneurysm by angiography, or other imaging modalities. The aneurysm is completely treated surgically, or even with use of endovascular techniques. The patient responds well clinically; awake, alert, and neurologically intact. One week later, he or she deteriorates and may be disabled or even die of the effects of cerebral vasospasm. Cerebral vasospasm is a reversible reduction in the caliber of the lumen of an artery in the subarachnoid space. The diagnosis of cerebral vasospasm is based on the angiographic image. It begins most often on day 3 after subarachnoid hemorrhage and reaches a maximum on days 6–8 (1). Symptoms are related to the region of cerebral ischemia and, if the vasospasm is severe enough, cerebral infarction can ensue. Whether the patient develops symptoms and infarction is related to many factors, including collateral flow, cardiac output, blood pressure, degree of any pre-existing arterial stenoses or occlusions, intracranial pressure, hyperglycemia, age, history of cigarette smoking, and the initial neurologic grade (2– 4). Cerebral vasospasm is the most frequent complication after subarachnoid hemorrhage. It is present angiographically in up to 70% of patients and is clinically symptomatic in 30% of patients (5). The International Cooperative Study on the timing of aneurysm surgery found vasospasm to be the leading cause of unfavorable outcomes resulting in death or disability in 13.5% of patients studied (6). The pathophysiology of cerebral vasospasm after subarachnoid hemorrhage is poorly understood. It is probably a combination of increased constrictor mechanisms and decreased dilator functions (7). It is well-accepted that the volume of subarachnoid blood on CT is the single best prognostic factor for forming vasospasm (8). It appears that some type or types of “spasmogens” are released from blood in the subarachnoid space. There is a vast array of possible agents within the blood stream and an even greater number when clotted blood, cerebrospinal fluid, and cerebral tissue are combined. Because vasospasm does not occur until 3 days after hemorrhage, it has been postulated that these agents are released from erythrocytes, which are broken down during that time period and tend to disappear from the cerebrospinal fluid in 2–3 weeks, the general time interval in which cerebral vasospasm tends to abate. Hemoglobin often has been implicated specifically as a triggering agent (9). There are morphologic and functional changes in the arterial wall of the vasospastic vessel that combine to cause sustained smooth muscle contraction exhausting the metabolic machinery of the cell, producing a type of rigor (10,11). When spasmogen levels eventually fall, the smooth muscle cells relax, abating the vasospasm. Treatment of cerebral vasospasm after subarachnoid hemorrhage falls into two major categories: medical therapy and endovascular therapy. Medical therapy for vasospasm is 1 From the Department of Radiology, Duke University Medical Center, Durham, North Carolina. Received September 15, 1999; revision requested November 4; revision received December 15; accepted December 16. Address correspondence to T.P.S., Department of Radiology, Room 1502, Duke University Medical Center, Erwin Rd., Durham, NC 27710; E-mail: smith146@mc.duke.edu