Unruptured Intracranial Aneurysms
Unruptured intracranial aneurysms (UIAs) constitute a significant public health issue. Several large autopsy studies have reported a wide range in the overall frequency of intracranial aneurysms, varying from 0.2% to 9.9%. More recent magnetic resonance angiography (MRA), angiography, and autopsy studies indicate an overall frequency of 2% to 6% among people over the age of 30 years, suggesting that among the U.S. population, at least 6 million people over the age of 30 years have or will have intracranial aneurysms.
The magnitude of the problem of UIAs is increasing as a result, at least in part, of the increasing age of the population, because these lesions generally develop with increasing age. In addition, in recent years, the widespread use of computed tomography (CT) and magnetic resonance imaging (MRI) has greatly increased the numbers of aneurysms that are discovered incidentally. The quality of these techniques has also improved, including MRA and computed tomographic angiography (CTA) studies, with high sensitivity and specificity for the detection of aneurysms larger than 3 mm in diameter.
Besides the fortuitous discovery of UIAs on CT, CTA, MRI, or MRA studies that are done for unrelated reasons, UIAs may be discovered when an evaluation is performed for a subarachnoid hemorrhage (SAH) from a different source, such as a separate aneurysm or an arteriovenous malformation (AVM), or investigates aneurysmal symptoms other than rupture. These symptoms include the following:
Cranial nerve palsies (most commonly cranial nerves II, III, IV, and VI)
Compression of other central nervous system structures (including the brainstem and the pituitary)
Persistent and often focal vascular headaches that are usually of relatively recent onset and new character
Focal ischemic symptoms from distal embolization of an aneurysmal clot
Seizure foci resulting from impingement on supratentorial brain structures.
Headache may be caused by a sudden dilation of the aneurysm or by chronic compression of pain-sensitive structures, such as the ophthalmic and maxillary divisions of the trigeminal nerve. Such headaches are usually persistent and focal, corresponding to the location of the aneurysm. They may also be associated with cranial nerve palsies. However, sudden and unusually severe headache associated with or without nausea or vomiting is always suspicious for a warning leak (or minor SAH) from an intracranial aneurysm. In these cases, CT or MRI studies should be performed, and if negative and no signs of mass effect exist, then lumbar puncture should be performed.
When decisions about management of UIAs need to be made, it is very important to recognize that ruptured intracranial aneurysms and UIAs constitute distinctly different clinical entities and need to be considered and treated as such. Previously ruptured intracranial aneurysms have a much greater likelihood of subsequent growth and rupture than do those that are previously unruptured. Furthermore, recent studies have confirmed that the natural history and behavior of UIAs cannot be extrapolated by looking at the characteristics of patients with aneurysms that are discovered after rupture. Much confusion regarding this issue has related to not recognizing the major differences between the following two questions: (1) What is the probability of a ruptured aneurysm being a certain size? (2) What is the probability of future rupture of a given-sized aneurysm discovered before rupture? The second of these questions is relevant to the clinical treatment of patients with UIAs. The key issue is that little is learned about the natural history of referring to characteristics of patients with ruptured aneurysms. This statement applies not only to aneurysm size but also to location. Available information suggests that most aneurysms that will rupture likely do so at the time they form or soon after and that the critical size for rupture is lower for aneurysms that rupture early.
Among patients with UIAs, there should be a distinction between patients without a history of SAH (group 1) and those with a history of SAH from a different source, most commonly another aneurysm that was successfully repaired (group 2).
Epidemiologic information from multiple vantage points suggests that most intracranial aneurysms that develop never rupture. It therefore is important to identify which unruptured aneurysms are at the greatest risk for subsequent rupture when deciding which ones to repair. Potential risk factors for rupture include aneurysm size, aneurysm location, selected morphology characteristics, aneurysmal growth, prior SAH, family history of SAH, cigarette smoking, and hypertension.1 Optimal medical care of patients with UIAs also involves predicting which patients will have the greatest likelihood of success and the lowest complication rates from repairing UIAs and reconciling these data with the natural history data involving UIAs and with the patients’ informed perspective regarding their desire to have the aneurysm treated.
A large international cohort study of UIAs, the International Study of Unruptured Intracranial Aneurysms (ISUIA) (Wiebers et al. 2003), included a large prospective natural history cohort and extensive outcomes information regarding open surgery and endovascular repair of UIAs. These ISUIA data allow an individualized, detailed assessment of the risks of natural history versus the risks of surgical and/or endovascular repair based on the additional information rather than just aneurysm size. Nonetheless, for group 1 patients with aneurysms less than 7 mm in diameter, it is unlikely that the natural history of these lesions can be improved, particularly in older patients, in those with aneurysms in the anterior circulation, and in those with aneurysms of very small size. Other factors to consider include family history, aneurysm morphology characteristics such as a daughter sac (i.e., a small protrusion off of the aneurysm dome), and aneurysm growth. For those with a family history of SAH, treatment of a UIA is reasonable, even in a smaller size than might be considered for repair in nonfamilial aneurysms. UIAs with a daughter sac are also considered for treatment; such a finding is uncommon in small UIAs but can occasionally occur. In addition, UIAs with clearly defined growth demonstrated on CTA or MRA should also be offered treatment unless significant comorbidities are present. The risk of aneurysm growth is dependent on aneurysm size,
but is occasionally detected in small aneurysms. It is important to note that available natural history studies, including ISUIA, have very few symptomatic patients with small UIAs, particularly those with acute or changing symptoms and most of these are considered for surgical or endovascular treatment.
but is occasionally detected in small aneurysms. It is important to note that available natural history studies, including ISUIA, have very few symptomatic patients with small UIAs, particularly those with acute or changing symptoms and most of these are considered for surgical or endovascular treatment.

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