Is reversible enlargement of the spinal cord a presyrinx state?

Mechanisms of syrinx formation have long attracted interest and speculation. Until recently, most believed that syringomyelia was caused by a forceful diversion of CSF from the fourth ventricle into the central canal of the spinal cord attributed to either obstruction of the outlets of the fourth ventricle (1) or the development of a pressure gradient between the intracranial and intraspinal compartments (2). This classical hypothesis, which shaped operative treatment for half a century and led to innovations in surgical technique such as ‘‘plugging the obex’’ to prevent syrinx filling, was quickly challenged after the introduction of MR imaging. Clinicians were quick to note that only a minority of syrinxes communicate directly with the fourth ventricle, and that most are separated from it by a long segment of syrinx-free spinal cord. The need to understand better the mechanisms of syrinx formation better has resulted in a quickening pace of research on many fronts. In this issue of the American Journal of Neuroradiology (page 7), Fischbein et al describe a presyrinx state that has potentially important etiologic and therapeutic implications. Syringomyelia can be classified into three general pathologic types: 1) central canal syrinxes that communicate with the fourth ventricle in association with hydrocephalus; 2) noncommunicating central canal syrinxes that occur with a wide variety of congenital and acquired disorders, including Chiari malformations, arachnoiditis, and extramedullary compressive lesions; and 3) parenchymal (extracanalicular) syrinxes that are found typically in the watershed area of the spinal cord and are associated with conditions that directly injure spinal cord tissue, such as trauma, infarction, and hemorrhage. Parenchymal syrinxes invariably produce neurologic deficits, whereas concentrically enlarged central canal syrinxes can be asymptomatic or produce only nonspecific neurologic findings unless the parenchyma of the spinal cord is dissected paracentrally. Precise clinicopathologic correlations can often be made on the basis of axial MR imaging with consecutive thin sections through the area of cavitation. A question of critical importance is How do syrinxes fill? Ball and Dayan (3), and subsequently Aboulker (4), were the first to suggest that syrinxes fill from the spinal subarachnoid space and that CSF enters the central canal through the dorsal