Jonathan L. Brisman, M.D., Joon K. Song, M.D., and David W. Newell, M.D.
From the Department of Cerebrovascular and Endovascular Neurosurgery, New Jersey Neuroscience Institute, JFK Medical Center, Edison, N.J. (J.L.B.); the Department of Endovascular Surgery, Institute forNeurology and Neurosurgery, Roosevelt Medical Center, New York (J.K.S.); and the Department of Neurosurgery, Seattle Neuroscience Institute, Swedish Medical Center, Seattle (D.W.N.). Address reprint requests to Dr. Brisman at the Department of Cerebrovascular and Endovascular Neurosurgery, New Jersey Neuroscience Institute at JFK Medical Center, Edison, NJ 08818, or at firstname.lastname@example.org. N Engl JMed 2006;355:928-39.
Copyright © 2006 Massachusetts Medical Society.
accular intracranial aneurysms, abnormal focal outpouchings of cerebral arteries, cause substantial rates of morbidity and mortality. Recently, major changes have occurred in the way we think about and treat this disease. Previous concepts about the natural history, particularly the risk of rupture of certain aneurysms, havebeen challenged.1,2 When this topic was the subject of a Medical Progress article in the Journal in 1997, minimally invasive percutaneous endovascular treatment of intracranial aneurysms (a technique known as coiling) had been introduced as an experimental procedure for patients who were not good candidates for surgery.3 After almost a decade of increased use and evaluation, endovascular coilinghas proved to be a safe and durable alternative to the traditional neurosurgical treatment of craniotomy and clip ligation (“clipping”). Coiling has now surpassed clipping as the primary method of treatment for intracranial aneurysms in some centers. Since the Guglielmi detachable coil for the treatment of intracranial aneurysms was approved in 1995 by the Food and Drug Administration (FDA), anestimated 150,000 patients have been treated with this device.4,5 In this article, the technological advances and supporting research contributing to this important change in practice patterns are reviewed.
EPIDE MIOL O GY A ND PATHOPH YSIOL O GY
Intracranial aneurysms are common lesions; autopsy studies indicate a prevalence in the adult population between 1 and 5 percent,2 whichtranslates to 10 million to 12 million persons in the United States.3 Fortunately, most aneurysms are small, and an estimated 50 to 80 percent of all aneurysms do not rupture during the course of a person’s lifetime.6 Intracranial aneurysms are considered to be sporadically acquired lesions, although a rare familial form has been described.3 Associated conditions include autosomal dominant polycystickidney disease, fibromuscular dysplasia, Marfan’s syndrome, Ehlers–Danlos syndrome type IV, and arteriovenous malformations of the brain. An estimated 5 to 40 percent of patients with autosomal dominant polycystic kidney disease have intracranial aneurysms,3,7 and 10 to 30 percent of patients have multiple aneurysms.3 Screening with intracranial magnetic resonance angiography is indicated for peoplewho have two immediate relatives with intracranial aneurysms and for all patients with autosomal dominant polycystic kidney disease.3,8,9 Rescreening of patients with autosomal dominant polycystic kidney disease is recommended, although the frequency of the procedure depends on whether other affected family members are known to have intracranial aneurysms.8 The estimated incidence of subarachnoidhemorrhage from a ruptured intracranial aneurysm in the United States is 1 case per 10,000 persons, yielding approximately 27,000 new cases of subarachnoid hemorrhage each year.3,5 Subarachnoid hemorrhage is more common in women than in men (2:1)10; the peak incidence
n engl j med 355;9
august 31, 2006
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