Antiphospholipid antibodies and stroke.

The clinical study of stroke is a recent occurrence. The clarion call awakening interest consisted of two reports that appeared during the years following World War II : the detailed description by Kubik and Adams [1) of the clinical and pathologic findings in patients with basilar artery occlusion, and C. Miller Fisher's monograph [2] directing attention to the signs and symptoms found in patients with carotid artery disease in the neck. During the next three decades, pathologists , clinicians, and radiologists worked to clarify the anatomy, pathology, and imaging features of strokes involving the large and small blood vessels of the brain. During the last decade, stroke clinicians have rediscovered that blood flows through the blood vessels. Diseases of the blood and blood vessels can cause or contribute to thromboembolism and bleeding, with resultant brain damage. Blood disorders in the most general sense are diseases detected or monitored by tests of the blood rather than imaging or sonographic studies of the anatomy and function of the brain and its vascular supply. During the past 5 years, many advances have been made in understanding the complex process of clot formation, clot lysis, and treatment of thrombosis. Table 1 lists broad categories of blood abnormalities that predispose to thrombosis and brain ischemia [3). In this issue of the AJNR, Pulpeiro and colleagues [4] discuss the MR findings in a patient with a syndrome in one of these categories of blood disorders: the antiphospholipid antibody (.A.PLA) syndrome, a type of immunological disorder that has recently received much attention [5-1 0). The nomenclature of the APLA syndrome is confusing. Antiphospholipid antibodies are immunoglobulins (lgG, lgM,