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Review Articles

Medical Progress

28 January 2, 1997

The New England Journal of Medicine

I

NTRACRANIAL

A

NEURYSMS

W

OUTER

I. S

CHIEVINK

, M.D.

From the Department of Neurologic Surgery, Mayo Clinic, 200 First St.SW, Rochester, MN 55905, where reprint requests should be addressed toDr. Schievink.

1997, Massachusetts Medical Society.

NTRACRANIAL aneurysms are acquired le-sions that are most commonly located at thebranching points of the major arteries coursing

through the subarachnoid space at the base of the

brain (Fig. 1). A subarachnoid hemorrhage due tothe rupture of an intracranial aneurysm is a devastat-ing event associated with high rates of morbidityand mortality. Approximately 12 percent of patientsdie before receiving medical attention,

1

40 percentof hospitalized patients die within one month afterthe event,

2-6

and more than one third of those whosurvive have major neurologic deficits.

2-6

Further-more, persistent cognitive deficits are present inmany patients otherwise considered to have a goodoutcome.

7,8

In spite of diagnostic, medical, and sur-gical advances over the past several decades, the casefatality rate for aneurysmal subarachnoid hemor-rhage has not changed.

5,6,9,10

In this review I discussrecent developments in our understanding of theepidemiology and pathogenesis of intracranial aneu-rysms, methods of diagnosis, and approaches totreatment.

EPIDEMIOLOGY

Prevalence of Intracranial Aneurysms

An intracranial aneurysm is a fairly common in-cidental finding at postmortem examination, with aprevalence ranging from 1 to 6 percent amongadults in large autopsy series.

11,12 Many of theseaneurysms, however, are very small, and the preva-lence of incidental intracranial aneurysms among

adults undergoing cerebral angiography is between0.5 and 1 percent.

13,14

These rates suggest that be-tween 1 million and 12 million Americans have in-tracranial aneurysms.

I

The majority of intracranial aneurysms (80 to 85

percent) are located in the anterior circulation, mostcommonly at the junction of the internal carotid ar-tery and the posterior communicating artery, theanterior communicating-artery complex, or the tri-furcation of the middle cerebral artery.

15,16

Aneu-rysms of the posterior circulation are most frequent-ly located at the bifurcation of the basilar artery orthe junction of a vertebral artery and the ipsilateralposterior inferior cerebellar artery.

15,16

Multiple in-tracranial aneurysms, usually two or three in number,are found in 20 to 30 percent of patients.

15-17

In rarecases, as many as 13 intracranial aneurysms have beendetected in a patient.

15,18

Incidence of Subarachnoid Hemorrhage

Aneurysmal subarachnoid hemorrhage is a majorclinical problem in the United States, with an annualincidence of approximately 1 per 10,000 people.

2,9

This rate suggests that each year approximately27,000 Americans have ruptured intracranial aneu-rysms, which are fatal in 14,000. The incidence ofaneurysmal subarachnoid hemorrhage is higher thanthat of many other major neurologic disorders, in-cluding primary brain tumors and multiple sclerosis(Table 1). Although the incidence of other types ofstroke (i.e., cerebral infarction and intracerebralhemorrhage) decreased substantially between the1950s and 1980s,

19

the incidence of aneurysmal

subarachnoid hemorrhage has not changed.

2,9

Patients who have had an aneurysmal subarach-noid hemorrhage are at increased risk for the devel-opment of a new aneurysm some time after the ini-tial aneurysm has been discovered. Each year, newaneurysms develop in at least 2 percent of patients

with previously ruptured aneurysms,

25

and in thisgroup of patients, the incidence of aneurysmal rup-ture is approximately 6 per 10,000 per year,

26,27

which is substantially higher than the incidence ofaneurysmal subarachnoid hemorrhage in the generalpopulation.

PATHOLOGICAL FEATURES

Aneurysms arising from the intracranial arteriesare much more common than those arising from ex-tracranial arteries of similar size. One possible reasonfor this discrepancy is that as compared with theirextracranial counterparts, intracranial arteries havean attenuated tunica media and lack an external elas-tic lamina. On microscopical examination, the typi-cal saccular, or berry, aneurysm has a very thin tuni-ca media or none, and the internal elastic lamina iseither absent or severely fragmented.

28,29

Thus, the

The New England Journal of MedicineDownloaded from nejm.org on May 27, 2013. For personal use only. No other uses without permission.

Copyright 1997 Massachusetts Medical Society. All rights reserved.

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29

wall of the aneurysm is generally composed of only

intima and adventitia, with variable amounts of fi-brohyaline tissue interposed between these two lay-ers.

28,29

Macroscopically, many intracranial aneurysms,especially those that rupture, have an irregular ap-pearance, with one or more daughter sacs and vari-able wall thickness. The point of rupture is generallyin the dome of the aneurysm.

PATHOGENESIS

Genetic Factors

Considerable evidence supports the role of ge-netic factors in the pathogenesis of intracranial an-eurysms. The two main lines of evidence are the as-sociation of intracranial aneurysms with heritableconnective-tissue disorders

30

and their familialoccurrence.

31

Of the numerous heritable connective-tissue disorders that have been associated withintracranial aneurysms, the most important are auto-somal dominant polycystic kidney disease, EhlersDanlos syndrome type IV, neurofibromatosis type 1,and Marfans syndrome.

30,31

It is not known to whatextent these specific heritable disorders are presentin the population of patients with intracranial aneu-rysms, but in one series of 100 consecutive patients

Figure 1.

Common Sites of Intracranial Aneurysms on the Circle of Willis at the Base of the Brain.

Anteriorcommunicatingartery

Posteriorcommunicating

artery

Anterior cerebralartery

Internal carotidartery

Posterior inferiorcerebellar artery

Vertebral artery

Basilar artery

Middle cerebralartery

Posterior cerebral

artery

*Data are from population studies in Rochester (Olmsted

County), Minnesota.

2,19-24

T

ABLE

1.

I

NCIDENCE

OF

S

ELECTED

M

AJOR

N

EUROLOGIC

D

ISORDERS

IN

THE

U

NITED

S

TATES

.*

D

ISORDER

A

NNUAL

I

NCIDENCE

(

PER

10,000P

ERSONS

)

Cerebral infarction 12.0Aneurysmal subarachnoid hemorrhage 1.0Bacterial meningitis 0.9Multiple sclerosis 0.6Intracranial glioma 0.5GuillainBarr syndrome 0.2

Amyotrophic lateral sclerosis 0.2



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with intracranial aneurysms, 5 had known heritableconnective-tissue disorders.

32

The true frequency ofheritable connective-tissue disorders among patients

with aneurysms is probably higher, for two reasons.First, these disorders often remain undiagnosed be-cause of substantial variability in their phenotypic

expression, and second, although many of the disor-ders are inherited in an autosomal dominant fashion,the family history is frequently negative because thedisease is caused by a new mutation. With the excep-tion of autosomal dominant polycystic kidney dis-ease, heritable connective-tissue disorders are rarelyidentified in families with intracranial aneurysms.

31

The familial aggregation of intracranial aneurysmswas first described in 1954 by Chambers et al.,

33

and hundreds of familial cases have since been re-ported.

31

Familial intracranial aneurysms are muchmore common than has generally been appreciated.

According to several epidemiologic studies, 7 to 20percent of patients with aneurysmal subarachnoid

hemorrhage have a first- or second-degree relativewith a confirmed intracranial aneurysm.

34-37

Recentstudies have also indicated that the familial aggre-gation of intracranial aneurysms is not a matter ofchance. Among first-degree relatives of patients

with aneurysmal subarachnoid hemorrhage, the riskof a ruptured intracranial aneurysm is approximatelyfour times higher than the risk in the general pop-ulation.

36-38

The risk may be highest among siblingsof index patients.

36

In most families with intracranialaneurysms, only two or three members are knownto be affected, and the inheritance pattern is un-clear.

31

In a segregation analysis of published pedi-grees, no single mendelian model but several possi-ble patterns of inheritance were identified, withautosomal transmission being the most likely.

31

Thissuggests that genetic heterogeneity is an importantfeature of intracranial aneurysms. As compared withsporadic intracranial aneurysms, familial aneurysmsrupture at an earlier age, may be smaller when theyrupture, and are more often followed by the forma-tion of a new aneurysm.

31,39,40

Affected siblings areoften in the same decade of life at the time of therupture.

39,40

Environmental Factors

Several lines of evidence suggest that acquired fac-tors have an important role in the pathogenesis ofintracranial aneurysms. For example, intracranial an-eurysms are very rare in children, and although themean age of patients with aneurysmal subarachnoidhemorrhage is only around 50 years, the incidenceof hemorrhage increases with age until at least theeighth decade of life.

2

Numerous casecontrol andlongitudinal studies have attempted to identify riskfactors for subarachnoid hemorrhage.

Of the various environmental factors that mayconfer a predisposition to aneurysmal subarachnoid

hemorrhage, cigarette smoking is the only factorthat has consistently been identified in all the popu-lations studied,

3,41-46

and it is also the most easilypreventable. The estimated risk of an aneurysmalsubarachnoid hemorrhage is approximately 3 to 10times higher among smokers than among nonsmok-

ers.

41-46

In addition, the risk increases with the num-ber of cigarettes smoked,

42,44,45

and patients whocontinue to smoke after an initial subarachnoidhemorrhage may be at especially high risk for thedevelopment of a new aneurysm.

47,48

It is unclearhow cigarette smoking affects the development ofaneurysms, but several hypotheses have been pro-posed. Cigarette smoking has been shown to de-crease the effectiveness ofa

1

-antitrypsin, the maininhibitor of proteolytic enzymes (proteases) such aselastase, and the imbalance between proteases andantiproteases in smokers may result in the degrada-tion of a variety of connective tissues, including thearterial wall.

32,49

In support of this hypothesis is the

observation that patients with a genetically deter-mined a

1

-antitrypsin deficiency may also be at in-creased risk for the development of intracranial an-eurysms.

32,49,50

Hypertension is the most frequently studied riskfactor for the development and rupture of intracra-nial aneurysms.

2,3,42-46,51-53Several studies have shownthat hypertension is associated with an increased riskof aneurysmal subarachnoid hemorrhage,

3,42-44,46

aswell as unruptured intracranial aneurysms.

52

Somestudies, however, have not shown an increasedrisk.

2,45,51

At autopsy, left ventricular hypertrophy isa common finding in patients with intracranial an-eurysms.

53

Although the data are inconsistent, takentogether they suggest that hypertension poses a riskof aneurysmal subarachnoid hemorrhage, but prob-ably not as high a risk as that associated with ciga-rette smoking.

The incidence of aneurysmal subarachnoid hem-orrhage, unlike other types of stroke, is higher among

women than among men.

2-4

Before the fifth decadeof life, however, aneurysmal subarachnoid hemor-rhage occurs more frequently in men, suggestingthe role of hormonal factors. The use of low-doseoral contraceptives by premenopausal women doesnot increase and may even decrease the risk ofsubarachnoid hemorrhage,

42,54,55

although in studiesperformed when oral contraceptives had a higher es-trogen content than they do now, the risk was sig-nificantly increased,

41,56

possibly because of the di-rect effect of estrogen on blood pressure. The risk ofaneurysmal subarachnoid hemorrhage is lower amongpostmenopausal women receiving hormone-replace-ment therapy than among postmenopausal womennot receiving such therapy,

54,57

but not as low as therisk among premenopausal women. These data sug-gest that premenopausal women have a low risk ofaneurysmal subarachnoid hemorrhage, postmeno-



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ceding the hemorrhage by several days or weeks.

63,64

Such a prodromal headache is most likely due to mi-nor leaking of blood into the wall of the aneurysmor into the subarachnoid space and is therefore com-monly referred to as a warning leak.

63,64

Theseprodromal headaches are often not recognized assuch by physicians, and many cases of frank aneurys-mal subarachnoid hemorrhage are initially misdiag-nosed as migraine headache, sinusitis, influenza, ormalingering.

65

Aneurysmal rupture may cause notonly subarachnoid hemorrhage but also intraventric-ular, intracerebral, or subdural hemorrhage (Fig. 2).It is rare for aneurysmal rupture to result in theseother types of intracranial hemorrhage without anyevidence of subarachnoid hemorrhage.

In addition to the global or focal neurologic ab-normalities that may be found on physical examina-tion, depending on the location and severity of thesubarachnoid hemorrhage, meningismus and intra-

ocular hemorrhages are two signs that are helpful inestablishing a clinical diagnosis of subarachnoid hem-orrhage. Signs of meningeal irritation are found inmost patients with aneurysmal subarachnoid hemor-rhage.

16

It is caused by the breakdown of blood prod-ucts within the subarachnoid space, and neck stiff-

ness may not develop until several hours after thehemorrhage. The subsequent circulation of bloodycerebrospinal fluid down the spinal axis may causesevere lower back pain and bilateral radicular legpain, sometimes overshadowing the head or neckpain. Ophthalmologic examination reveals unilateralor bilateral subhyaloid hemorrhages in approximate-ly one fourth of patients with aneurysmal subarach-noid hemorrhage.

66

These hemorrhages are venousin origin and are located between the retina and vit-reous membrane. Because subhyaloid hemorrhagesare gravity-dependent, they are convex at the bot-tom and flat at the top (Fig. 3).

The most important predictor of the outcome of

subarachnoid hemorrhage is the patients clinicalcondition on arrival at the hospital.

2

Numerousgrading systems for subarachnoid hemorrhage havebeen proposed over the years, but the scale devel-oped by the World Federation of Neurological Sur-geons

67

(based in part on the Glasgow Coma Scale

68

)has gained universal acceptance and is used most

widely (Table 2).

Mass Effect

Some intracranial aneurysms become symptomaticbecause of a mass effect (Fig. 4). Such aneurysms areoften, but not invariably, large or giant.

69

The mostcommon symptom of an aneurysmal mass effect isheadache, and the most common sign is a palsy ofthe third nerve caused by an aneurysm at the junc-tion of the carotid artery and the posterior commu-nicating artery or an aneurysm of the upper end ofthe basilar artery. Characteristically, the third-nervepalsy involves the pupillary fibers. Depending on thelocation of the aneurysm, other manifestations of amass effect include brain-stem dysfunction, visual-field defects, trigeminal neuralgia, a cavernous sinussyndrome, seizures, and hypothalamicpituitary dys-function. Unruptured intracranial aneurysms causinga mass effect carry a high risk of subsequent rupture,

with an estimated frequency of 6 percent per year.

70

Cerebral Ischemia

Cerebral ischemic symptoms referrable to the vas-cular territory distal to an aneurysm may in rare cas-es be the presenting clinical manifestation of an un-ruptured intracranial aneurysm.

69,71

Such ischemia isbelieved to be caused by the embolization of an in-traaneurysmal thrombus, and it should be distin-guished from intracranial arterial dissection with thesecondary formation of an aneurysm, which typical-ly presents with cerebral symptoms.72

Figure 3. Funduscopic Photograph of a Subhyaloid Hemor-rhage in the Right Eye of a 45-Year-Old Woman with a Rup-

tured Aneurysm of the Middle Cerebral Artery.

*The scale was developed by the World Federationof Neurological Surgeons. Data are adapted from

Drake.67The score is derived from the Glasgow Coma

Scale, as described by Teasdale and Jennett.68

TABLE 2. GRADING SCALE FORSUBARACHNOIDHEMORRHAGE.*

GRADE

GLASGOWCOMA

SCORE MOTOR DEFICIT

I 15 AbsentII 13 or 14 AbsentIII 13 or 14 PresentIV 712 Absent or presentV 3 6 Absent or present



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Asymptomatic Intracranial Aneurysms

The discrepancy between the prevalence of inci-dental intracranial aneurysms at autopsy and the in-cidence of aneurysmal subarachnoid hemorrhage in-dicates that most aneurysms never rupture. Similarly,in large autopsy series the majority of intracranialaneurysms are unruptured and apparently have nevercaused any symptoms.11 With the widespread useof computed tomographic (CT) scanning and mag-netic resonance imaging (MRI), many unrupturedasymptomatic intracranial aneurysms can now be de-tected. The natural history of such aneurysms is in-completely understood, but all the large studies havereported annual rupture rates of 0.5 to 2 per-cent.25,70,73,74 The rate of rupture increases with thesize of the aneurysm but appears to be unrelated tothe age or sex of the patient or to the presence orabsence of hypertension.70 Data presented by Wie-bers and colleagues suggest that only intracranial an-eurysms that are 10 mm or larger in diameter carrya significant risk of subsequent rupture,70 but thereis still considerable controversy about the size below

which the risk of rupture is negligible.25,75,76

Diagnostic Studies

Subarachnoid Hemorrhage

CT scanning should be the first diagnostic studyperformed to evaluate the possibility of a subarach-noid hemorrhage (Fig. 5). CT scans are very sensi-tive in detecting acute hemorrhage, and they candemonstrate the presence of a subarachnoid hemor-rhage in 90 to 95 percent of patients who undergoscanning within 24 hours after the hemorrhage.16,77

Blood is cleared rapidly from the subarachnoidspace, however, and the sensitivity of CT scanningdecreases to 80 percent at three days, 70 percent atfive days, 50 percent at one week, and 30 percent attwo weeks.16,77 CT scans are also very useful in de-tecting any associated intracerebral hemorrhage orhydrocephalus, and the distribution of blood mayoffer important clues to the location of the rupturedaneurysm (Fig. 5).

If there is a strong clinical suspicion of a subarach-noid hemorrhage but the CT scan is normal, then alumbar puncture should be performed. Bloody cer-ebrospinal fluid may be caused by a traumatic lum-bar tap, and a decrease in the red-cell count from thefirst to the last tube is an unreliable basis for rulingout a subarachnoid hemorrhage.78 Xanthochromia(yellow discoloration) of the supernatant after cen-trifugation of the cerebrospinal fluid, however, is di-agnostic of a subarachnoid hemorrhage. Xantho-chromia is caused by the breakdown of bloodproducts in the cerebrospinal fluid, and it takes sev-eral hours for those blood products to break downand circulate to the lumbar theca. A lumbar punc-ture performed very soon after the subarachnoid

hemorrhage may therefore fail to show xanthochro-mia.78 With the use of spectrophotometry, xantho-chromia is detected in all patients with subarachnoidhemorrhage between 12 hours and 2 weeks after thehemorrhage and is still detectable in more than 70percent of patients after 3 weeks and in 40 percentafter 4 weeks.78 In most hospital laboratories, how-ever, xanthochromia is determined by visual inspec-tion alone and not by spectrophotometry, makingthe detection of the abnormality less reliable.

MRI is not sensitive in detecting acute hemor-rhage, and its role in the early evaluation of sub-arachnoid hemorrhage is limited. However, MRI

Figure 4. Mass Effect from Intracranial Aneurysms.

A midsagittal section through the brain of a 54-year-old man

shows a giant (4.5 cm) aneurysm of the basilar artery that iscompressing the medulla and pons (Panel A). A coronal sec-tion through the brain of a 55-year-old man shows an unrup-

tured, 9-mm aneurysm of the right internal carotid artery thatis compressing the right optic nerve and chiasm (Panel B).

A

B



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may be very useful in demonstrating subacute orchronic subarachnoid hemorrhage long after thefindings on the CT scan have become normal.79

Intracranial Aneurysms

The three most commonly used techniques to di-

agnose an intracranial aneurysm are conventionalangiography, MRI angiography, and helical (spiral)CT angiography (Fig. 6). Because of its unsurpassedresolution, conventional angiography remains themethod of choice for detecting an intracranial aneu-rysm and determining its anatomical characteristics.

Although the risks associated with conventional an-giography are very low, they are not negligible. Suchrisks include cerebral infarction, the formation of ahematoma or pseudoaneurysm at the puncture site,and renal failure. In most large series, the mortalityrate is less than 0.1 percent, and the rate of perma-nent neurologic injury is approximately 0.5 per-cent.80 The majority of complications in these series

occur in elderly persons with severe atheroscleroticdisease, not in patients with intracranial aneurysms.However, the risk associated with angiography is ex-ceedingly high in some groups of patients with in-tracranial aneurysms (e.g., those with generalizedconnective-tissue disorders such as the EhlersDan-los syndrome).30

Because it does not require the intravascular ad-ministration of contrast material, MRI angiographyis the most convenient diagnostic study and carriesessentially no risk. Nowadays, MRI angiographycan detect intracranial aneurysms as small as 2 or3 mm in diameter, but in prospective studies thecritical size for detection is about 5 mm.81,82 Thus,some small aneurysms will be missed with MRI an-giography. Although it is the most commonly useddiagnostic study in screening for intracranial aneu-rysms, MRI angiography is only rarely sufficient forsurgical planning. Standard MRI is the best meth-od for demonstrating the presence of a thrombus

within the aneurysmal sac. Although uncommon,there have been several instances of thrombosed in-tracranial aneurysms that were not visualized onangiography but were clearly demonstrated withMRI.83,84

Recently, helical CT angiography has been usedto detect intracranial aneurysms, and preliminary re-ports indicate that the detection rate with this tech-nique is similar to that with MRI angiography.85,86

An advantage of helical CT angiography in surgicalplanning is its ability to demonstrate the relation ofthe aneurysm to the bony structures of the skullbase. Helical CT angiography is also useful in screen-ing for new aneurysms in patients with initial aneu-rysms that were treated with ferromagnetic clips;these older clips are an absolute contraindication toMRI angiography. However, MRI can be performedsafely in patients who have the more common, non-

Figure 5. CT Images of Aneurysmal Subarachnoid Hemor-rhage.

A CT scan in a 55-year-old woman shows subarachnoid blood

within the interpeduncular and ambient cisterns and the rightsylvian fissure, caused by a ruptured aneurysm at the junctionof the right carotid artery and the posterior communicating ar-

tery (Panel A). A CT scan in an 82-year-old woman shows ex-tensive subarachnoid blood within the cortical sulci, intraven-tricular hemorrhage, and an intracerebral hematoma adjacent

to a large, ruptured aneurysm of the anterior communicatingartery (Panel B).

A

B



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ferromagnetic metallic clips. Conventional CT scan-ning is the preferred method for detecting calcifica-tions within the wall of the aneurysm.

Screening

Screening for asymptomatic intracranial aneu-rysms appears to be warranted, because aneurysmalsubarachnoid hemorrhage has a dismal prognosis,

whereas the treatment of most asymptomatic intra-cranial aneurysms is associated with a fairly low rateof morbidity (less than 5 percent) and mortality(less than 2 percent).76,87 However, the natural his-tory of asymptomatic intracranial aneurysms is not

well defined, and the benefits of screening have nev-er been quantified. A possible caveat for screeningprograms is based on evidence that intracranial an-eurysms may develop over a short period (months,

weeks, or even days) and either rupture immediatelyor remain fairly stable without rupturing.69,88,89

Screening has been suggested for patients at highrisk for the development of an aneurysm. The twogroups of patients most commonly screened are those

with a family history of intracranial aneurysms31,89,90and those with autosomal dominant polycystic kid-ney disease.91-95 In the absence of any clinical featureor biologic marker that can identify persons in

whom intracranial aneurysms are most likely todevelop, screening is generally recommended forasymptomatic members of families with two or moreaffected members.31,90 Although the extent of screen-ing depends on the apparent inheritance pattern ina particular family, usually only first-degree relativesare screened. Using such a screening program, Ron-kainen and colleagues detected asymptomatic intra-cranial aneurysms in 37 of 396 persons (9 percent)

with affected family members.90 Some investigatorshave suggested screening of persons with only a sin-gle affected family member.38 However, the absolutelifetime risk of subarachnoid hemorrhage for per-sons with one affected first-degree relative is small(1 percent at the age of 50 and 2 percent at the ageof 70), even though they have a risk of aneurysmalrupture that is four times higher than that in thegeneral population.36 Screening is therefore not rec-ommended for such persons.

Approximately 5 to 10 percent of asymptomaticadults with autosomal dominant polycystic kidneydisease who undergo screening are found to havesaccular intracranial aneurysms.91-93 Clustering of in-tracranial aneurysms has been reported in severalfamilies with autosomal dominant polycystic kidneydisease, and screening reveals asymptomatic aneu-

Figure 6. Arteriogram (Panel A), MRI Angiogram (Panel B), and Helical CT Angiogram (Panel C) Showing an Unruptured Aneurysmat the Vertebrobasilar Junction in a 41-Year-Old Woman.

A B C



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Figure 7. Treatment of Intracranial Aneurysms by Surgical Clipping or Endovascular Coiling.

Lateral carotid subtraction angiograms in a 35-year-old woman show a 17-mm supraclinoid aneurysm of the carotid artery beforetreatment (Panel A) and after the placement of a single, straight SundtKees clip (Panel B). Anteroposterior vertebral subtractionangiograms in a 53-year-old woman show a 13-mm basilar aneurysm before treatment (Panel C) and after the placement of four

Guglielmi detachable coils with a total length of 90 cm (Panel D). The densely compacted coils are more easily seen on a plainskull radiograph (Panel E).

A

C D E

B



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rysms in 20 or 25 percent of the members of suchfamilies.92,93 Therefore, although screening for asymp-tomatic intracranial aneurysms in patients with auto-somal dominant polycystic kidney disease remainscontroversial, most investigators agree that screeningis indicated for those patients who also have family

histories of intracranial aneurysms.91-95

TREATMENT

The ultimate goal of treatment is to exclude theaneurysmal sac from the intracranial circulation

while preserving the parent artery. Treatment of in-tracranial aneurysms has long been the domain ofneurosurgeons, but since 1990, neuroradiologistshave been using endovascular techniques to treat in-creasing numbers of patients with intracranial aneu-rysms.

Surgery

The placement of a clip across the neck of an in-

tracranial aneurysm is the most definitive treatmentand, because of its proven long-term efficacy, re-mains the treatment of choice (Fig. 7A and 7B). In1936, Walter Dandy performed the first plannedsurgical repair of an intracranial aneurysm by placinga silver clip, designed by Harvey Cushing, across theneck of an aneurysm at the junction of the carotidartery and the posterior communicating artery in apatient with a painful third-nerve palsy.96 Surgicaltechniques for repairing intracranial aneurysms haveimproved tremendously since then, particularly overthe past two decades, with the introduction of mi-crosurgical techniques, the operating microscope,bipolar coagulation, and a variety of self-closing an-eurysm clips.97,98 Nowadays, clipping of most intra-cranial aneurysms carries a fairly low risk directly at-tributable to the surgery. Some aneurysms are notamenable to safe direct clipping because of theirsize, location, or configuration, and sophisticatedadjunctive techniques, such as vascular bypass graft-ing or hypothermic cardiac arrest, must be used.97-99In spite of the availability of these techniques, someintracranial aneurysms are best treated by surgical orendovascular occlusion of the proximal vessel.100

An area of continuing controversy in the manage-ment of ruptured intracranial aneurysms is the tim-ing of surgery. Early surgery (i.e., within 48 to 72hours after the hemorrhage) is beneficial because pa-tients with subarachnoid hemorrhage are at veryhigh risk for a recurrent hemorrhage shortly afterthe initial one. The rate of recurrent hemorrhageis at least 4 percent within the first 24 hours101 (andmay be as high as 10 or 20 percent102,103) and be-tween 1 and 2 percent per day for the first 2 weeks.101Early surgery also allows aggressive treatment of thesecondary intracranial arterial narrowing, or vaso-spasm, which is an important cause of delayed cere-bral ischemia after subarachnoid hemorrhage.104 The

cause of vasospasm is not known, but its incidenceis clearly related to the amount of subarachnoidblood seen on the CT scan.104 Vasospasm occurs be-tween 3 and 15 days after the subarachnoid hemor-rhage, and the optimal treatment hypervolemia,hypertension, intraarterial papaverine infusion, or

endovascular balloon angioplasty is dangerous inthe presence of an untreated ruptured aneurysm.104Because of brain edema and the presence of a tena-cious clot around the aneurysm, however, early sur-gery may be technically more challenging than sur-gery performed 10 to 14 days after the hemorrhage.

Although the approach to patients with subarach-noid hemorrhage who are in poor clinical condition(grade IV or V in Table 2) varies widely from oneinstitution to another, most neurosurgeons recom-mend early aneurysmal repair in patients with sub-arachnoid hemorrhage who are in good clinical con-dition (grade I or II). Moreover, several groups havereported good results with early surgery in patients

who are in poor clinical condition.105,106 Emergencysurgery is indicated in patients who have a majormass effect from an intracerebral or subdural he-matoma.

Endovascular Therapy

Endovascular treatment is emerging as a promis-ing alternative to surgical clipping in selected casesof intracranial aneurysm.107-109 The initial experience

with endovascular therapy, in which a detachableballoon was used to occlude an intracranial aneu-rysm, was disappointing because of arterial ruptureand deflation of the balloon. Current endovasculartherapy involves the insertion of soft metallic coils

within the lumen of the aneurysm, which are de-tached once they have been satisfactorily placed (Fig.7C, 7D, and 7E).107-109 Then, through the process ofelectrothrombosis, a local thrombus forms aroundthe coils within the aneurysm.107 The goal of endo-

vascular coiling is complete obliteration (i.e., throm-bosis) of the aneurysmal sac. Many factors affect theobliteration rate, but the most important factor isthe ratio of the neck of the aneurysm to the fun-dus.108,109 Aneurysms with wide necks are less ame-nable to endovascular treatment than those withnarrow necks, because with a wide-necked aneu-rysm, the coils tend to compact into the body anddome of the aneurysm, resulting in an aneurysmremnant and incomplete treatment. The early expe-rience with coil embolization for the treatment ofintracranial aneurysms suggests that the proceduralrisks are fairly low, but the long-term effectivenesshas not yet been proved.108,109

The disadvantages of early surgery in patients withruptured intracranial aneurysms are of minor impor-tance in endovascular treatment. Some patients maytherefore best be treated with emergency endovas-cular coiling of the dome of the aneurysm, which



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provides at least temporary protection against recur-rent hemorrhage and allows aggressive treatment of

vasospasm, followed by definitive surgical clipping, ifthe aneurysm cannot be completely obliterated. En-dovascular treatment of intracranial aneurysms isevolving rapidly, and the proportion of patients with

intracranial aneurysms who are best treated with en-dovascular coiling, alone or in combination withsurgery, remains to be determined.

I am indebted to Drs. Michael J. Link, Douglas A. Nichols, andDavid G. Piepgras for their critical reading of the manuscript andto Mr. David A. Factor for the drawing in Figure 1.

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