Annals of Indian Academy of Neurology
  Users Online: 1864 Home | About the Journal | InstructionsCurrent Issue | Back IssuesLogin      Print this page Email this page  Small font size Default font size Increase font size

REVIEW ARTICLE
Year : 2007  |  Volume : 10  |  Issue : 1  |  Page : 12-20
 

Incidental intracranial aneurysm


Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India

Correspondence Address:
S Nair
Department of Neurosurgry, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram - 695 011, Kerala
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.31480

Rights and Permissions

 

   Abstract 

The management of of unruptured intracranial aneurysms is one of the most important issues confronting neurosurgeons today. The high mortality and morbidity associated with subarachnoid hemorrhage (SAH) has prompted interest in repair of aneurysms that are discovered before they have ruptured. A strong risk factor for intracranial aneurysm which causes SAH is a positive family history, polycystic kidney disease and patients who have survived a SAH. There is no cutoff size of aneurysm below which rupture is not possible. Presently there are no definitive guidelines in the management of incidental aneurysms and many centers consider each case individually with treatment offered for lesions more than 7 mm in diameter especially if patient is relatively young without major co-morbidities. Even though microsurgery offers the advantage of proven durability and higher rates of total aneurysm obliteration, the choice of treatment modality between open microsurgery and endovascular occlusion is flexibly adjusted to each case.


Keywords: Incidental aneurysm, unruptured aneurysm


How to cite this article:
Nair S, Menon G, Rao B, Khurshid, Rajesh B J, Mathew A, Easwer H V. Incidental intracranial aneurysm. Ann Indian Acad Neurol 2007;10:12-20

How to cite this URL:
Nair S, Menon G, Rao B, Khurshid, Rajesh B J, Mathew A, Easwer H V. Incidental intracranial aneurysm. Ann Indian Acad Neurol [serial online] 2007 [cited 2019 Nov 20];10:12-20. Available from: http://www.annalsofian.org/text.asp?2007/10/1/12/31480



   Introduction Top


The morbidity and mortality associated with aneurysmal subarachnoid hemorrhage remain distressingly high despite advances in microneurosurgery, interventional radiology, neuroanaesthesia and critical care. Although intracranial aneurysms are common affecting 5% of the population,[1] the incidence of subarachnoid hemorrhage is relatively low (approximately 1 case per 10,000 persons per year),[2] especially in patients with small (<10 mm in diameter) aneurysms, suggesting that most aneurysms do not rupture. A great number of unruptured and often incidental intracranial aneurysms is being diagnosed today because of the increasing age of the population and improvements in imaging techniques. Patients harboring a unruptured intracranial aneurysm (UIA) are potentially at high risk of dying from subarachnoid hemorrhage (SAH). Prevention of this rupture with surgical or endovascular treatment is believed to be the most effective strategy to prevent mortality and morbidity. However, all current treatments carry some risks and therefore the natural history of UIAs must be considered carefully, before formulating treatment recommendations. The decision to treat or not to treat is important because treatment-related complications usually occur at or around the time of the procedure. Therefore, the cumulative lifetime risk for rupture of an untreated aneurysm needs to be evaluated to make a judgement of what is best for the patient. Also one should know the factors associated with risk of intracranial aneurysm formation and subarachnoid hemorrhage and identify the subset of people who need to be screened for incidental aneurysms. With a thirty day mortality rate following rupture reaching 50% with nearly half the survivors having irreversible brain damage1,[3] it is understandable that discovery of UIAs should prompt enthusiasm for expeditious treatment. There are many growing controversies about incidental aneurysms (1) Should we screen for incidental intracranial aneurysms in people at risk of harboring them? (2) When is it appropriate to secure an incidental anenurysm? (3) What are the risks of rupture if aneurysm is not treated? (4) If the treatment is pursued, what treatment modality to be used? To answer the above questions and to obtain a rationale for management of UIAs, one should have an idea of its formation. Majority of aneurysms are saccular in shape and result from a combination of factors including degeneration and weakening of the internal elastic lamina and collagen fibers of the arterial wall as well as hemodynamic effects of fluid pulsations. Factors associated with risk of intracranial aneurysm and subarachnoid hemorrhage can be classified as modiable and nonmodifiable.[4] The major identified modifiable risk factors include active smoking, hypertension, excessive alcohol consumption and possibly the use of oestrogens.[5],[6],[7],[8],[9] Some case control studies also found increased risk with intake of coffee and use of cocaine.[9] The most important unchangeable risk factors are familial occurrence of SAH and autosomal dominant polysystic kidney disease (ADPKD).[10],[11] Aneurysms have also been associated with connective tissue diseases such as  Ehlers-Danlos syndrome More Details type IV, neurofibromatosis and Marfan disease, but these disorders are rare and therefore the number of patients with SAH related to them is small.[12]


   Population at Risk Top


A family history of SAH is the strongest risk factor and is defined as having at least one first degree relative (parent, sibling, child) with SAH. However, because such a family history is not common, screening of people who have a family history of SAH will not have a large effect on the incidence of SAH.[4] The chance of having an aneurysm and the life time risk of SAH depend on the number of affected first degree relatives.[10],[11] The life time risk of SAH in individuals with two or more affected first-degree relatives is unknown because there are few families with this history and because those that exist tend to seek screening for aneurysms and treatment of those detected. The chance of an aneurysm depends not only on the number of affected relatives, but also on the relationships. If the affected relatives are siblings, the risk of having an aneurysm is higher than if they are parents or children.[10],[11] Aneurysms are more commonly large and multiple in familial than in sporadic SAH.[13] However, because only 10% of cases of SAH are associated with a family history, large and multiple aneurysms are more commonly seen in sporadic than in familial SAH. Patients with familial SAH tend to be younger than sporadic cases and in families with two generations affected the age at onset is earlier in the younger than in older generation.[14],[15] Risk of intracranial aneurysms and of SAH according to the number of affected first degree relatives shows that individuals with one affected relative have a 5.5 times greater life-time risk of SAH than the general population.[10],[11] But the risk of finding an aneurysm with screening in an individual with one affected relative is only 1.7 times higher than in the general population.[10],[11] This suggests that the familial intracranial aneurysms have a higher risk of rupture and the rate of development of new aneurysms is quicker in relatives with familial occurrence of SAH than in individuals without familial occurrence. People with two or more affected relatives and with negative result on magnetic resonance angiography have a 7% risk of developing an aneurysm within five years of screening.[16]

Although SAH is common in patients with ADPKD, less than 1% cases of SAH are attributable to ADPKD because the disease is rare.[17] Intracranial aneurysms are found in about 10% of patients with ADPKD.[10] Apart from a positive family history for SAH, no clinical characteristics have been identified that are associated with increased risk of aneurysm in patients with ADPKD. The position of the mutation in PKD1 is predictive of development of aneurysms, but mutation detection is not yet used in clinical practice. As for people with a positive family history of intracranial aneurysms, people with ADPKD are at risk of developing new aneurysms.[10]

Patients who have been successfully treated for an aneurysm are at risk of developing new aneurysms.[18],[19],[20] There are only few series, all with short follow-up, which have reported the risk of development of denovo aneurysms. In these reports the rate of development of new aneurysms was between 0.4% and 2.2% per year.[18],[19],[20] Apart from development of new aneurysms, an occluded aneurysm might reopen or a new aneurysm could develop at the site of a treated aneurysm. The rate of growth of aneurysms after clipping was about 0.5% per year in two series with high rates of follow-up angiography.[18],[19] In two follow-up studies, the risk of recurrent SAH after clipping was estimated to be 2% in 10 years and about 9% in 20 years, which is about 30-50 times higher than the risk in the general population.[18],[20] A higher proportion of patients with two occurrences of SAH had a positive family history of the disorder (30%) than those with SAH in general (10%).[11] Patients with recurrence of SAH were also younger at onset than those with the disorder in general. The mean time between the first and second episodes was 7.8 years, ranging from 2.8 to 14 years for SAH from denovo aneurysm.[21],[22] The lower limit of about 3 years for a new episode from a denovo aneurysm accord with other studies on rupture of de-novo aneurysms. A new aneurysm seems to take some time to develop, although some case reports have described rupture of new aneurysms within two to six months after initial SAH.[22],[23]

International study of unruptured intracranial aneurysms (ISUIA) study and controversies

Asymptomatic unruptured aneurysm, which constitute between 17-37% of all unruptured aneurysms, are less prone to bleeding than symptomatic unruptured aneurysms.[1],[24],[25] Their annual bleeding rate has been the focus of much controversy. Most of this controversy stems from the results of the ISUIA which were first published in 1998.[1] The ISUIA had two objectives. The first was to evaluate the natural history of UIA and the second was to establish the risk of treatment. The study consisted of retrospective and prospective components. In the retrospective component, the natural history of UIAs was evaluated and in the prospective component, the morbidity and mortality-related to treatment were evaluated. A total of 1449 patients with 1937 UIAs were included in the retrospective cohort. They were divided into two groups: 727 patients of group 1 who had no prior history of SAH and the 722 patients of group 2 who had history of SAH. The mean duration of follow-up was 8.3 years. Of the 1449 patients, 32 had documented aneurysmal rupture. In group 1, the cumulative rate of rupture was 0.05% per year for aneurysms less than 10mm in diameter and about 1% in those over 10 mm in diameter. Aneurysms larger than 25 mm had a 6% rupture rate in the first year. In group 2, the cumulative rate of rupture was about 0.5% per year for lesions smaller than 10 mm and about 1% for those larger than 10 mm in diameter. In group 1, in addition to size, location was related to hemorrhage risk, with basilar top, vertebrobasilar, posterior cerebral and posterior communicating artery aneurysms having a higher risk of rupture. In group 2, only location (i.e., basilar top) and increasing age predicted an increased risk of hemorrhage. The risks of ISUIA study, however, was lower than what previous studies had suggested.[26],[27],[28] Jane and coauthors estimated that the long-term risk of rupture for an incidentally discovered cerebral aneurysm was between 1% and 2% per year.[28] Similarly, Juvela et al found the annual rupture risk to be 1.4% per year among 181 untreated aneurysms followed in 132 Finnish patients over a 30 year period. The annual risk to patients was 2.1% because some patients had more than one aneurysm.[26],[29] Results of the initial report of the ISUIA have created much controversy and the study has been criticized based on select nature of the retrospective cohort and the comparison between the prospectively gained morbidity data and the very low rupture rate for patients in the historical cohort who had been selected for non-operative intervention. It was suggested that the retrospective group had excluded patients with the highest risk of rupture and introduced data-collection bias, artificially lowering the estimated annual hemorrhage rate and those patients enrolled in ISUIA were preselected for low natural history risk and these low-risk patients represented only about 2% of the patients seen in practice.[30],[31],[32] This combined retrospective/prospective ISUIA report did not make clear distinction between the risks of symptomatic and truly incidental unruptured aneurysms and did not determine the influence of genetic factors, smoking history or concurrent diseases such as ADPKD. Subsequently in a population based study by Juvela et al , 142 unselected patients from a defined geographic area were observed for an average of 20 years. The risk of hemorrhage was 1.3% and each millimeter increase in aneurysm size was associated with an increase of 1.11 in the relative risk of hemorrhage.[29] In addition active cigarette smoking was found to be an important predictor of aneurysm rupture. This study along with another study from Japan[24] suggest that risk of rupture from asymptomatic aneurysms is probably closer to 1% than 0.1% per year and this risk is highly dependent on age, smoking, lesion size and lesion location. Surgical series show that multiple aneurysms represent about a third of unruptured aneurysms. The annual risk of bleeding of an unruptured aneurysm discovered during angiography performed for a ruptured aneurysm in another location is greater than the risk for an isolated asymptomatic lesion.[33],[34] In the ISUIA, prior SAH was associated with an 11 fold increase in rupture for small (<10 mm) aneurysms.[35] No additional risk was observed for larger aneurysms. The exact additional risk of rupture of an asymptomatic aneurysm when there is a history of SAH is not certain.

There is considerable documentation in literature that the majority of the ruptured aneurysms are smaller than 10 mm. In the cooperative aneurysm study angiographic studies revealed a mean maximal diameter of 8.23.9 mm and a median diameter of 7 mm.[36] Seventy one percent of the sacs were smaller than 10 mm and 13% were less than 5 mm in diameter. The relationship between aneurysm size and hemorrhage from unruptured aneurysm is not fully elucidated. According to an international study of unruptured intracranial aneurysms, in patients with no history of subarachnoid hemorrhage, the five year cumulative rate of rupture of aneurysms located in the internal carotid artery, anterior communicating artery, anterior cerebral artery or middle cerebral artery is zero for aneurysms under 7 mm, 2.6% for 7 to 12 mm, 14.5% for 13 to 24 mm and 40% for 25 mm or more.[37] This rate is in contrast to rupture rates of 2.5%, 14.5%, 18.4% and 50%, respectively, for the same sizes of aneurysms in the posterior circulating and posterior communicating artery. Some authors suggest that unruptured aneurysms less than 10 mm in diameter do not bleed even though the average size of[38] ruptured aneurysm from the same group was 7.5 mm.[39],[40] Yasui et al followed 25 unruptured aneurysms including 66% that were less than 5mm at the time of detection. Twenty five percent of the aneurysms were still less than 5mm when SAH occurred.[38] In a prospective population based study an association between increased aneurysm size and bleeding was observed.[26] The median diameter of unruptured aneurysms that subsequently bled was no different from the median diameter of those that did not rupture (4 mm). In the same study, aneurysm growth on serial examination was associated with an increased risk of bleeding. The available data suggests that whereas increased aneurysm size is associated with increased risk of rupture, small aneurysms certainly bleed and in some patients this risk of bleeding may be predicted by aneurysm growth.

Results of a continuation of the prospective arm of ISUIA have recently been published.[37] Compared with rupture rates in the retrospective cohort, rupture rates were higher in patients from group 1 (no prior SAH) of the prospective cohort who had unruptured aneurysms of at least 7 mm in diameter and this difference was most pronounced for for aneurysms 7-9 mm in diameter. Size had little predictive value in patients with history of SAH from a different aneurysm (group 2). On multivariate analysis age >50 years, aneurysm size >12 mm, posterior circulation location, previous ischaemic cerebrovascular disease and aneurysm symptoms other than rupture were[37] predictive of poor outcome after craniotomy while in patients treated endovascularly,[37] only size >12 mm and posterior circulation location were associated with poor outcome. Comparison between the surgical and endovascular groups is not possible because of the unbalanced distribution of patients in the treatment groups of this nonrandomized study. There was a high rate of incomplete aneurysm obliteration in patients who underwent endovascular therapy[37] although the overall treatment related morbidity and mortality at one year was lower in the endovascular group.

Should we screen for incidental aneurysms

The benefits of screening for asymptomatic intracranial aneurysms have never been quantified. No clinical trials have been done on screening for aneurysms in patients at increased risk and presumably such trials will not be done because the follow-up needs to be 20 years or longer. The goal of screening is not to detect or to treat an aneurysm, but to increase the number of quality years of life. Decisions therefore must be made from calculations and assumptions about perceived quality of life.[4] Definitely patient gets a reassurance with a negative screening result, but it can also cause anxiety if a 3 mm aneurysm is found and left untreated or if an unrelated abnormality is found.[41] Also one has to bear in mind that even repeated screening and preventive treatment cannot prevent all episodes of SAH because in rare instances aneurysms can develop and rupture within the regular screening interval of five years.[42] Conventional angiography, however, is not useful for screening high risk groups because a single negative angiogram does not exclude the possibility of a de novo lesion developing in future. MRA is at present the most satisfactory technique for screening high risk groups. The number of false negatives may be reduced by the simultaneous use of CT angiography. Screening should be done in individuals with two or more affected first-degree relatives and in patients with ADPKD. With this screening strategy, approximately 10% of individuals are found to have an intracranial aneurysm.[43],[44],[45],[46] In approximately a third of these patients, the aneurysms are larger than 5mm in diameter.[43] Because aneurysms are very rare before the age of 20 years, screening is started after this age. If a first screening is negative, repeated screening should be advised, because the risk of finding an aneurysm five years after the initial screening is about seven percent.[16] Screening should not be advised if the life expectancy of the patient is short because of advanced age or comorbid illness and the maximum age for screening is 60-70 years depending on individuals health status.[4] Screening should also be done in identical twins if SAH has occurred in one of the twins. In many pairs, the aneurysms are at the same site and SAH tends to occur at around the same age.[47],[48] In individuals with only one affected first-degree relative, screening is not very reliable or effective as relatives of index SAH cases have only a 4% risk of harboring an intracranial aneurysm and this low incidence may not make screening cost-effective.[49],[50] To prevent one episode of fatal SAH, 300 at risk people must be screened.[4] The general advice is not to screen individuals with only one affected relative. Patients with Ehlers-Danlos syndrome type IV are advised against screening because of the fragility of the vessel wall which substantially increases risk of treatment.[51] There is no indication for screening patients with neurofibromatosis or Marfan disease because an increased risk of SAH has not been confirmed in these groups.[4] Patients who have had an aneurysmal SAH are at increased risk for development of a new aneurysm some time after the initial aneurysm has been discovered. Each year, risk of new aneurysm to develop is at least 2% of patients with previously ruptured aneurysms and in this group of patients, the incidence of aneurysmal rupture is approximately 6 per 10,000 per year, which is substantially higher than the incidence of aneurysmal SAH in the general population.[26] Follow-up screening of aneurysms in this group might be beneficial, but evidence to advise follow-up screening in such patients is insufficient.


   Management Issues Top


We know that rate of rupture of UIA is affected by factors such as aneurysm size, aneurysm location, multiplicity of aneurysms, aneurysmal growth, symptomatic aneurysms and patient factors such as age, gender and history of hypertension and smoking. The presence of severe progressive symptoms from an aneurysm within the subarachnoid space is an indication for treatment, regardless of the size of the unruptured aneurysm. Symptomatic unruptured aneurysms often require treatment because of headaches, cranial nerve deficit, seizures and embolic stroke. The risk of bleeding also is greater in symptomatic unruptured than asymptomatic unruptured aneurysms.[37] Symptomatic lesions represent about a third of all unruptured lesions, but account for three quarters of the cases that bleed during observation. Overall, the risk of complications from treatment is around 5% risk of death or persisting impairment in activities of daily living and 10% for persisting cognitive deficits or reduced quality of life.[37] The risks are higher for neurosurgical clipping than for endovascular coiling, especially in patients older than 50 years.[37],[52],[53],[54] The complication rates are probably lower for aneurysms detected by screening, because they are mostly small and risks of complication from treatment increase with size of aneurysms.[55] In a meta-analysis by Raaymakers and coworkers, in which the treatment of 2568 unruptured aneurysms in 2460 patients was examined the surgical morbidity was 10.9% and mortality 2.6%.[52] Similarly, in the prospective arm of the ISUIA, among 996 patients undergoing surgery, one year mortality was 2% in patients with previous SAH and 3.8% in patients without prior history of SAH.[37] The morbidity for both groups was approximately 12% and much of the morbidity included subclinical neuropsychological defects that had limited the functional impact. The meta-analysis of Raaymakers et al had several caveats because studies varied inclusion criteria, inconsistent outcome measures, unclear information about neurosurgeon's experience and a relatively high percentage (37%) of symptomatic unruptured aneurysms included in the analysis. In addition, there were a relatively large number of giant and posterior circulation aneurysms, both have particularly poor surgical outcomes. When these two groups of patients were analysed separately, Raaymakers and coworkers[52] found that the surgical mortality and morbidity among other aneurysms were 0.8% and 1.9% respectively. To date, the most selective meta-analysis of unruptured aneurysm surgery was performed by King and associates,[56] who observed an overall mortality rate of 1% and morbidity of 4.1 percent. This study, unlike the meta-analysis by Raaymakers included more aneurysms less than 10 mm in diameter (72% versus 54%) and more aneurysms located in the anterior circulation (94% versus 70%).[56]

Factors associated with surgical outcome

Increased aneurysm size is the most important factor associated with surgical complications and poor outcome. Aneurysms larger than 25 mm in diameter have a fourfold increased risk compared with 5 mm aneurysms.[57] Wirth et al showed operative morbidity following surgery of 2% for aneurysms smaller than 5mm, 7% for aneurysms 6 to 15 mm and 14% for aneurysms between 16 to 25 mm.[58] Among 92 unruptured giant aneurysms at Columbia Presbyterian Hospital, morbidity reported in 25% and overall 83% experienced a good or excellent outcome, while for lesions less than 10 mm, 99% had good or excellent outcome.[55] Ninety nine percent of nongiant and 90% of the giant aneurysm patients returned to work. Aneurysm size was also related with technical results with only 60% of giant lesions undergoing clip occlusion while it was 85% for lesions less than 10 mm diameter.[59] The association between increased aneurysm size and poor outcome may be explained in part by the aneurysm's intimate association with small perforators, broad aneurysm neck, intraluminal thrombosis or atherosclerosis in aneurysm neck or dome. In the series of Wirth et al[58] aneurysm location affected outcome in anterior circulation aneurysms; morbidity was 5% for posterior communicating aneurysms, 8% for middle cerebral aneurysms, 12% for ophthalmic lesions, 16% for anterior communicating lesions and 17% for internal carotid bifurcation lesions. A similar relationship between anterior circulation aneurysm location and outcome was not observed by the Columbia Presbyterian hospital group.[59] In their observation basilar bifurcation lesions were associated with poor outcome and worse angiographic result with only 66% having angiographic occlusion. But 81% experienced a good or excellent outcome in this group. Even though advanced age is recognized as a poor prognostic indicator for surgery, many surgeons have reported good surgical results in patients older than 60 years.[55],[58],[60] Wide aneurysm necks reduce the success of endovascular procedures but is generally less significant in surgery. Calcification in aneurysm neck is associated with increased surgical difficulty and is also associated with an increased incidence of cerebral embolism and intraoperative bleeding from aneurysm neck. Patient related factors including advanced age, ischemic cerebrovascular disease and medical conditions such as diabetes mellitus also increase the risk of unruptured aneurysm surgery.

Endovascular treatment

In some patients, endovascular coil occlusion is a valuable alternative to surgery in the treatment of unruptured aneurysm, even though the long term effect on natural history remains uncertain. Also there are difficulties in evaluating coil embolization technology because the procedure is constantly being refined and additional experience gained. Procedural morbidity with this technique is between 6 to 19% in the older series with overall favorable outcome in 82% and a mortality of ten percent.[61],[62],[63] Endovascular procedures appear to be less successful than surgical procedures in occluding unruptured aneurysm with only 50% achieving complete occlusion.[61],[62] A second limitation to endovascular procedure is aneurysm recurrence which is between 16 to 32 percent.[59] The results of GDC embolization for incidentally discovered, unruptured aneurysms were assessed in a series of 120 patients by Murayama and colleagues.[64] Thirty nine percent of the aneurysms were ophthalmic segment aneurysms and 18% were located at basilar bifurcation. Complete GDC occlusion could be achieved in only 63% of cases and procedure related morbidity was 5.2 percent. Follow-up angiograms were available in only 77 patients of the original 120 patient cohort. After the original embolization, complete occlusion was observed in 52 aneurysms and a small neck remnant was visualized in 22 aneurysms. At follow-up angiography, none of the 52 completely occluded aneurysms had recanalised. In the 22 aneurysms with small neck remnants, 8(36%) showed aneurismal recanalization due to coil compaction. A comparative study by Johnston and coworkers in a cohort of patients treated at 60 university hospitals from January 1994 through June 1997, using the University Health System Consortium database, looked at the outcome between coil embolization and surgical clipping for both symptomatic and incidental unruptured aneurysms.[65] Adverse outcomes were significantly more common in surgical cases (18.5%) than in endovascular cases (10.6%). In another study, Johnston and colleagues[59] compared 130 cases ideal for either technique that underwent surgery or coil embolization during a 10 year period. Surgical complications were threefold greater than endovascular complications probably because the surgical team did not have a dedicated cerebrovascular surgeon and low volume surgical centers were compared with high volume endovascular centers.

Management guidelines for incidental aneurysms

Whether or not to treat a truly incidental (asymptomatic) aneurysm remains controversial. It is clear that size of the aneurysm is important; however, it is also clear that there is no cutoff size below which rupture is not possible. Small aneurysms have a risk of hemorrhage even though this risk may be less than that of larger aneurysms. In general, the risk that small aneurysms (<7 mm) will rupture is low, particularly if they are on the anterior circulation. Small aneurysms might therefore best be left untreated.[37] However, this approach is not appropriate for patients who have two or more relatives who died from SAH. Several studies have reported a higher risk of rupture for familial than for sporadic aneurysms.[10] Patients with unruptured aneurysms, whose relatives have died from SAH, know that the hemorrhages occurred from small aneurysms. A patient with a small aneurysm but a positive family history is difficult to reassure with general statements that small aneurysms have a low risk of rupture. In patients with small aneurysms (<7 mm), the decision on whether or not to treat depends on age of the patient, site of the aneurysm, accessibility of the aneurysm for coiling in older patients, whether or not a previous SAH has occurred and the ability to cope with the knowledge of having an untreated aneurysm.[4] In patients with very small aneurysms (3 mm or less), follow-up assessment to check whether or not the aneurysm is increasing over the time seems to be a reasonable approach. The optimum period between follow-up assessments and the duration of follow-up are not known. At the University of Miami School of Medicine, each case of incidental aneurysm is considered individually and the treatment offered accordingly.[66] They recommend the treatment of incidental aneurysms that are more than 7 mm in diameter if the patient is relatively young and without major co-morbidities. If the patient is very young or has a family history of aneurysms or has had a SAH from another aneurysm, they recommend treatment even for aneurysms of a significantly smaller size. With larger aneurysms, they stretch the indications for treatment and treat patients who are older, but in relatively good medical health or younger patients with some comorbidities who are still likely to tolerate general anesthesia. Because of location and configuration, the decision making becomes more problematic for truly incidental large and giant aneurysms, where risk of treatment is very high. In such cases they consider age an important factor and tend to take risk in a younger patient and to observe an older patient with periodic imaging. A more aggressive approach is pursued if prominent growth of the aneurysm is seen on follow-up imaging. They also address the issue of treating incidental aneurysm with open microsurgery or endovascular occlusion. With unruptured aneurysm one does not have the problem of swollen, hyperemic and friable brain that may be injured by retraction at surgery and also there is no problem of vasospasm that may be exacerbated by surgery. Therefore they tend to lean more toward open microsurgery under equal circumstances with unruptured incidental aneurysms, because of the uncertainty about the long-term durability of coiling as opposed to microsurgical clipping in experienced hands. They recommend open microsurgical clipping for most aneurysms of the anterior circulation and for vertebral artery including origin of PICA or distal PICA or distal AICA aneurysms and aneurysms at the origin of superior cerebellar artery. For most basilar aneurysms they recommend endovascular treatment. As suggested by this group, it is very important to emphasize that the evaluation of "risk versus benefit" is an ongoing processthat continues until aneurysm is secured by either coiling or clipping. If one finds during surgery unexpected circumstances that clearly increase the risk of treatment, one should not hesitate to back off as may be seen in open surgery when the aneurysm neck is found calcified or if surgeon finds vital perforators that cannot be saved. Under such circumstances, the authors' advice to back off and either treat the patient conservatively or recommend endovascular therapy.


   The American Heart Association Guidelines Top


Members of the Stroke Council[67] recommended that the incidental aneurysms smaller than 10 mm in patients without a previous SAH should be observed rather than treated unless the patient is young, there is a daughter aneurysm or if there are unique hemodynamic features. Patients with a family history of aneurismal SAH also deserve special consideration for treatment. Aneurysms larger than 10 mm should be considered for treatment depending on age, health and aneurysm risk factors.

Advances

Recent advances in molecular genetics have made linkage studies possible to map the chromosomal locus of a putative intracranial aneurysm gene mutation. One approach is to screen the human genome for intracranial aneurysm genes by testing linkage of a large number of distinct highly polymorphic genetic markers. Another method for studying linkage is to analyze variations in the sharing of marker alles among affected sibling pairs only. Polymorphisms of several genes have now been investigated in patients with intracranial aneurysms. Certain polymorphisms of the angiotensin I connvering enzyme, matrix metalloproteinases and endoglin genes may be associated with an increased risk for aneurysm development.[68],[69],[70] Olson and colleagues[71] performed a sibling-pair linkage analysis in Finnish patients with intracranial aneurysms and identified a susceptibility locus at 19q13.1-13.3.


   Conclusion Top


The advent of reliable noninvasive imaging and efficacy of treatment for incidental cerebral aneurysm has awakened an interest in medical fraternity in the management of these patients. The numbers of incidental aneurysms will continue to increase as age of the population increases. The treating physician must understand the natural history to assess the effectiveness of treatment options. Whether or not it is proper to screen for incidental aneurysms is based on an understanding of aneurysm formation and rupture. If aneurysms develop over a brief period of time frame and are most prone to rupture during this period, aneurysm screening programs, will identify only stable aneurysms and miss the unstable ones that require treatment. If the long term risk of hemorrhage from an incidentally detected aneurysm is as low as that reported by ISUIA, treatment in its current form may pose greater risk to patients than does the disease itself. Treatment of incidental aneurysms will continue to evolve. The development of intravascular stents and flow redirectors may improve the result of endovascular procedures. Less invasive surgical approaches, better neuroprotection that permits longer temporary occlusion times and endoscopic instruments designed to identify perforators will similarly improve surgical results. The patients should have a management plan that is individualized and should consider the age of the person, life expectancy, comorbidities and characteristics of the aneurysm[72].

 
   References Top

1.Unruptured intracranial aneurysms-risk of rupture and risks of surgical intervention. International Study of Unruptured Intracranial Aneurysms Investigators. N Engl J Med 1998;339:1725-33.  Back to cited text no. 1    
2.Ingall TJ, Whisnant JP, Wiebers DO, O'Fallon WM. Has there been a decline in subarachnoid hemorrhage? Stroke 1989;20:718-24.  Back to cited text no. 2  [PUBMED]  
3.Mayer SA, Kreiter KT, Copeland D, Bernardini GL, Bates JE, Peery S, et al . Global and domain-specific cognitive impairment and outcome after subarachnoid hemorrhage. Neurology 2002;59:1750-8.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Rinkel GJ. Intracranial aneurysm screening: Indications and advice for practice. Lancet Neurol 2005;4:122-8.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Teunissen LL, Rinkel GJ, Algra A, van Gijn J. Risk factors for subarachnoid hemorrhage: A systematic review. Stroke 1996;27:544-9.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Qureshi AI, Suri MF, Yahia AM, Suarez JI, Guterman LR, Hopkins LN, et al . Risk factors for subarachnoid hemorrhage. Neurosurgery 2001;49:607-13.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Kissela BM, Sauerbeck L, Woo D, Khoury J, Carrozzella J, Pancioli A, et al . Subarachnoid hemorrhage: A preventable disease with a heritable component. Stroke 2002;33:1321-6.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Anderson CS, Feigin V, Bennett D, Lin RB, Hankey G, Jamrozik K, et al . Active and passive smoking and the risk of subarachnoid hemorrhage: An international population based case control study. Stroke 2004;35:633-7.  Back to cited text no. 8    
9.Broderick JP, Viscoli CM, Brott T, Kernan WN, Brass LM, Feldmann E, et al . Major risk factors for aneurysmal subarachnoid hemorrhage in the young are modifiable. Stroke 2003;34: 1375-81.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Rinkel GJ, Djibuti M, Algra A, van Gijn J. Prevalence and risk of rupture of intracranial aneurysms: A systematic review. Stroke 1998;29:251-6.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Bromberg JE, Rinkel GJ, Algra A, Greebe P, van Duyn CM, Hasan D, et al . Subarachnoid haemorrhage in first and second degree relatives of patients with subarachnoid haemorrhage. BMJ 1995;311:288-9.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Schievink WI, Prakash UB, Piepgras DG, Mokri B. Alpha 1 antitrypsin deficiency in intracranial aneurysms and cervical artery dissection. Lancet 1994;343:452-3.  Back to cited text no. 12  [PUBMED]  
13.Ruigrok YM, Rinkel GJ, Algra A, Raaymakers TW, Van Gijn J. Characteristics of intracranial aneurysms in patients with familial subarachnoid hemorrhage. Neurology 2004;62:891-4.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Bromberg JE, Rinkel GJ, Algra A, van Duyn CM, Greebe P, Ramos LM, et al . Familial subarachnoid hemorrhage: distinctive features and pattern of inheritance. Ann Neurol 1995;38: 929-34.  Back to cited text no. 14  [PUBMED]  
15.Struycken PM, Pals G, Limburg M, Pronk JC, Wijmenga C, Pearson PL, et al . Anticipation in familial intracranial aneurysms in consecutive generations. Eur J Hum Genet 2003;11:737-43.   Back to cited text no. 15  [PUBMED]  [FULLTEXT]
16.Wermer MJ, Rinkel GJ, van Gijn J. Repeated screening for intracranial aneurysms in familial subarachnoid hemorrhage. Stroke 2003;34:2788-91.   Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Gieteling EW, Rinkel GJ. Characteristics of intracranial aneurysms and subarachnoid hemorrhage in patients with polycystic kidney disease. J Neurol 2003;250:418-23.   Back to cited text no. 17  [PUBMED]  [FULLTEXT]
18.David CA, Vishtech AG, Spetzler RF, Lemole M, Lawton MT, Partovi S. Late angiographic follow-up review of surgically treated aneurysms. J Neurosurg 1999;91:396-401.  Back to cited text no. 18    
19.Tsutsumi K, Ueki K, Morita A, Usui M, Kirino T. Risk of aneurysm recurrence in patients with clipped aneurysms: Results of long-term follow-up angiography. Stroke 2001;32:1191-4.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: A long term follow-up study. Stroke 2001;32:485-91.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]
21.Tsutsumi K, Ueki K, Usui M, Kwak S, Kirino T. Risk of recurrent subarachnoid hemorrhage after complete obliteration of cerebral aneurysms. Stroke 1998;29:2511-3.   Back to cited text no. 21  [PUBMED]  [FULLTEXT]
22.Nakase H, Kamada Y, Aoki H, Goda K, Morimoto T, Sakaki T. Clinical study on recurrent intracranial aneurysms. Cerebrovas Dis 2000;10:255-60.  Back to cited text no. 22    
23.Yasuhara T, Tamiya T, Sugiu K, Inoue S, Ohmoto T. De novo formation and rupture of an aneurysm: Case report. J Neurosurg 2002;97:697-700.  Back to cited text no. 23  [PUBMED]  
24.Tsutsumi K, Ueki k, Morita A, Kirino T. Risk of rupture from incidental aneurysms. J Neurosurg 2000;93:550-3.  Back to cited text no. 24  [PUBMED]  
25.Bererstein A, Flamm ES, Kupersmith MJ. Unruptured intracranial aneurysms. N Engl J Med 1999;340:1439-42.  Back to cited text no. 25    
26.Juvela S, Porras M, Heiskanen O. Natural history of unruptured intracranial aneurysms: A long term follow-up study. J Neurosurg 1993;79:174-82.  Back to cited text no. 26  [PUBMED]  
27.Mount LA, Brisman R. Treatment of multiple aneurysms: Symptomatic and asymptomatic. Clin Neurosurg 1974;21:166-70.  Back to cited text no. 27  [PUBMED]  
28.Jane JA, Kassell NF, Torner JC, Winn HR. The natural history of aneurysms and arteriovenous malformations. J Neurosurg 1985;62:321-3.  Back to cited text no. 28  [PUBMED]  
29.Juvela S, Porras M, Poussa K. Natural history of unruptured aneurysms: Probability of and risk factors for aneurysm rupture. J Neurosurg 2000;93:379-87.   Back to cited text no. 29  [PUBMED]  
30.Dumont AS, Lanzio G, Kassell KF. Unruptured aneurysms. J Neurosurg 2002;96:52-60.  Back to cited text no. 30    
31.Juvela S. Unruptured aneurysms. J Neurosurg 2002;95:58-60.  Back to cited text no. 31    
32.Piepgras DG. Unruptured aneurysms. J Neurosurg 2002;96:63.  Back to cited text no. 32  [PUBMED]  
33.Heiskanen O. Risk of bleeding from unruptured aneurysms in cases with multiple intracranial aneurysms. J Neurosurg 1981;55:524-6.  Back to cited text no. 33  [PUBMED]  
34.Winn HR, Almaani WS, Berga SL, Jane JA, Richardson AE. The long term outcome in patients with multiple aneurysms. Incidence of late hemorrhage and implications of treatment of incidental aneurysms. J Neurosurg 1983;59:642-51.  Back to cited text no. 34    
35.Kataoka K, Taneda M, Asai T, Yamada Y. Difference in nature of ruptured and unruptured cerebral aneurysms. Lancet 2000;355:203.  Back to cited text no. 35    
36.Kassel NF, Torner JC. Size of intracranial aneurysms. Neurosurgry 1983;12:291-7.  Back to cited text no. 36    
37.Wiebers DO, Whisnant JP, Huston J 3rd, Meissner I, Brown RD Jr, Piepgras DG, et al . Unruptured intracranial aneurysms: Natural history, clinical outcome and risks of surgical and endovascular treatment. Lancet 2003;362:103-10.  Back to cited text no. 37  [PUBMED]  [FULLTEXT]
38.Yasui N, Magarisawa S, Suzuki A, Nishimura H, Okudera T, Abe T. Subarachnoid hemorrhage caused by previously diagnosed, previously ruptured intracranial aneurysms: A retrospective analysis of 25 cases. Neurosurgery 1996;39:1096-101.  Back to cited text no. 38  [PUBMED]  [FULLTEXT]
39.Wiebers DO, Whisnant JP, Sundt TM Jr, O'Fallon WM. The significance of unruptured intracranial saccular aneurysms. J Neurosurg 1987;66:23-9.  Back to cited text no. 39  [PUBMED]  
40.Piepgras DG. Management of incidental intracranial aneurysms. Clin Neurosurg 1989 ;35 :511-8.  Back to cited text no. 40  [PUBMED]  
41.van der Schaaf IC, Brilstra EH, Rinkel GJ, Bossuyt PM, van Gijn J. Quality of life, anxiety and depression in patients with an untreated intracranial aneurysm or arteriovenous malformation. Stroke 2002;33:440-3.  Back to cited text no. 41  [PUBMED]  [FULLTEXT]
42.Schievink WI, Limburg M, Dreissen JJ, Peeters FL, ter Berg HW. Screening for unruptured familial intracranial aneurysms: Subarachnoid hemorrhage 2 years after angiography negative for aneurysms. Neurosurgery 1991;29:434-8.  Back to cited text no. 42  [PUBMED]  
43.Ronkainen A, Hernesniemi J, Puranen M, Niemitukia L, Vanninen R, Ryynanen M, et al . Familial intracranial aneurysms. Lancet 1997;349:380-4.  Back to cited text no. 43  [PUBMED]  [FULLTEXT]
44.Brown BM, Soldevilla F. MR angiography and surgery for unruptured familial intracranial aneurysms in persons with a family history of cerebral aneurysms. AJR 1999;173:133-8.  Back to cited text no. 44  [PUBMED]  
45.Ronkainen A, Puranen MI, Hernesniemi JA, Vanninen RL, Partanen PL, Saari JT, et al . Intracranial aneurysms: MR angiographic screening in 400 asymptomatic individuals with increased familial risk. Radiology 1995;195:35-40.  Back to cited text no. 45  [PUBMED]  
46.Raaymakers TW, Rinkel GJ, Ramos LM. Initial and follow-up screening for aneurysms in families with familial subarachnoid hemorrhage. Neurology 1998;51:1125-30.  Back to cited text no. 46  [PUBMED]  
47.Ohno S, Ikeda Y, Onitsuka T, Nakajima S, Uchino H, Haraoka J, et al . Cerebral aneurysms in identical twins. No Shinkei Geka 2004;32:875-9.  Back to cited text no. 47  [PUBMED]  
48.Puchner MJ, Lohmann F, Valdueza JM, Siepmann G, Freckmann N. Monozygotic twins not identical with respect to the existence of intracranial aneurysms: A case report. Surg Neurol 1994;41:284-9.  Back to cited text no. 48  [PUBMED]  
49.Raaymakers TW. Aneurysms in relatives of patients with subarachnoid hemorrhage: Frequency and risk factors. MARS Study Group. Magnetic Resonance Angiography in Relatives of patients with Subarachnoid hemorrhage. Neurology 1999;53:982-8.  Back to cited text no. 49    
50.Yoshimoto Y, Wakai S. Cost-effectiveness analysis of screening for asymptomatic, unruptured intracranial aneurysms. A mathematical model. Stroke 1999;30:1621-7.  Back to cited text no. 50    
51.North KN, Whiteman DA, Pepin MG, Byers PH. Cerebrovascular complications in Ehlers-Danlos syndrome type IV. Ann Neurol 1995;38:960-4.  Back to cited text no. 51  [PUBMED]  
52.Raaymakers TW, Rinkel GJ, Limburg M, Algra A. Mortality and morbidity of surgery for unruptured intracranial aneurysms: A meta-analysis. Stroke 1998;29:1531-8.  Back to cited text no. 52  [PUBMED]  [FULLTEXT]
53.Raaymakers TW. Functional outcome and quality of life after angiography and operation for unruptured intracranial aneurysms. J Neurol Neurosurg Psychiatry 2000;68:571-6.  Back to cited text no. 53  [PUBMED]  [FULLTEXT]
54.Brilstra EH, Rinkel GJ, van der Graaf Y, Sluzewski M, Groen RJ, Lo RT, et al . Quality of life after treatment of unruptured intracranial aneurysms by neurosurgical clipping or by embolization with coils: A prospective, observational study. Cerebrovasc Dis 2004;17:44-52.  Back to cited text no. 54  [PUBMED]  [FULLTEXT]
55.Solomon RA, Fink ME, Pile-Spellman J. Surgical management of unruptured intracranial aneurysms. J Neurosurg 1994;80:440-6.  Back to cited text no. 55  [PUBMED]  
56.King JT Jr, Berlin JA, Flamm ES. Morbidity and mortality from elective surgery for asymptomatic, unruptured, intracranial aneurysms: A meta-analysis. J Neurosurg 1994;81:837-42.  Back to cited text no. 56  [PUBMED]  
57.Khanna RK, Malik GM, Qureshi N. Predicting outcome following surgical treatment of unruptured intracranial aneurysms: A proposed grading system. J Neurosurg 1996;84:49-54.  Back to cited text no. 57  [PUBMED]  
58.Wirth FP, Laws ER Jr, Piepgras D, Scott RM. Surgical treatment of intracranial aneurysms. Neurosurgery 1983;12:507-11.  Back to cited text no. 58  [PUBMED]  
59.Connolly ES Jr, Solomon RA. Management of unruptured aneurysms. In : Le Roux PD, Winn HR, Newell DW, editors. Management of cerebral aneurysms. Saunders: Philadelphia; 2004. p. 271-85.  Back to cited text no. 59    
60.Samson DS, Hodosh RM, Clark WK. Surgical management of unruptured symptomatic aneurysms. J Neurosurg 1977;46:731-4.  Back to cited text no. 60    
61.Cognard C, Pierot L, Boulin A, Weill A, Tovi M, Castaings L, et al . Intracranial aneurysms: Endovascular treatment with mechanical detachable spirals in 60 aneurysms. Radiology 1997;202:783-92.  Back to cited text no. 61  [PUBMED]  
62.Malisch TW, Guglielmi G, Vinuela F, Duckwiler G, Gobin YP, Martin NA, et al . Intracranial aneurysms treated with Guglielmi detachable coil: Midterm clinical results in a consecutive series of 100 patients. J Neurosurg 1997;87:176-83.  Back to cited text no. 62  [PUBMED]  
63.Pierot L, Boulin A, Castaings L, Rey A, Moret J. The endovascular approach in the management of patients with multiple intracranial aneurysms. Neuroradiology 1997;39:361-6.  Back to cited text no. 63  [PUBMED]  [FULLTEXT]
64.Murayama Y, Vinuela F, Duckwiler GR, Gobin YP, Guglielmi G. Embolization of incidental cerebral aneurysms by using the Guglielmi detachable coil system. J Neurosurg 1999;90:207-14.  Back to cited text no. 64  [PUBMED]  
65.Johnston SC, Dudley RA, Gress DR, Ono L. Surgical and endovascular treatment of unruptured cerebral aneurysms at university hospitals. Neurology 1999;52:1799-805.  Back to cited text no. 65  [PUBMED]  [FULLTEXT]
66.Baskaya MK, Jea A, Heros RC. Management of incidental aneurysms and vascular malformations. In : Rabinstein AA, Wijdicks EF, editors. Tough Calls in Acute Neurology. Butterworth-Heinemann: Philadelphia; 2004. p. 177-98.  Back to cited text no. 66    
67.Bederson JB, Awad IA, Wiebers DO, Piepgras D, Haley EC Jr, Brott T, et al . Recommendations for the management of patients with unruptured intracranial aneurysms: A statement for healthcare professionals from the Stroke Council of the American Heart association. Stroke 2000;31:2742-50.  Back to cited text no. 67  [PUBMED]  [FULLTEXT]
68.Takenaka K, Sakai H, Yamakawa H, Yoshimura S, Kumagai M, Yamakawa H, et al . Polymorphism of the endoglin gene patients with intracranial saccular aneurysms. J Neurosurg 1999;90:935-8.  Back to cited text no. 68  [PUBMED]  
69.Takenaka K, Yamakawa H, Sakai N, Yoshimura S, Murase S, Okumura A, et al . Angiotensin I-converting enzyme gene polymorphism in intracranial saccular aneurysm individuals. Neurol Res 1998;20:607-11.  Back to cited text no. 69    
70.Zhang B, Dhillon S, Geary I, Howell WM, Iannotti F, Day IN, et al . Polymorphisms in matrix metalloproteinase-1, -3, -9 and -12 genes in relation to subarachnoid hemorrhage. Stroke 2001;32:2198-202.  Back to cited text no. 70  [PUBMED]  [FULLTEXT]
71.Olson J, Vongpunsawad S, Kuivaniemi H. Genome scan for intracranial aneurysm susceptibility loci using finnish family. Am J Hum Genet 1998;63:A17.  Back to cited text no. 71    
72.Kobayashi S, Orz Y, George B, Lee KC, Alexander MJ, Spetzler RF, et al . Treatment of unruptured cerebral aneurysms. Surg Neurol 1999;51:355-62.  Back to cited text no. 72  [PUBMED]  [FULLTEXT]



This article has been cited by
1 Magnetic Resonance Angiography of the Circle of Willis in Patients with Symptomatic Intracranial Neuropathology: Medicare LCD L25367(R4)
John W. Gilbert, G. R. Wheeler, G. E. Mick, S. L. Herder, G. B. Richardson, B. B. Storey, P. G. Broughton, C. M. Kenney III
Journal of Neuroimaging. 2011; : no
[VIEW] | [DOI]



 

Top
Print this article  Email this article
Previous article Next article

    

 
   Search
 
   Next article
   Previous article 
   Table of Contents
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (184 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
    Introduction
    Population at Risk
    Management Issues
    The American Hea...
    Conclusion
    References

 Article Access Statistics
    Viewed7129    
    Printed161    
    Emailed1    
    PDF Downloaded318    
    Comments [Add]    
    Cited by others 1    

Recommend this journal