Intracranial aneurysm

Short description: Ballooning or rupturing of a blood vessel in the brain

Intracranial aneurysm

Other names| Cerebral aneurysm, brain aneurysm
Aneurysm of the basilar artery and the vertebral arteries
Symptoms| None, severe headache, visual problems, nausea and vomiting, confusion[1]
Usual onset| 30–60 years old
Causes| Hypertension, infection, head trauma[2]
Risk factors| old age, family history, smoking, alcoholism, cocaine use[1]
Diagnostic method| Angiography, CT scan
Treatment| Endovascular coiling, surgical clipping, cerebral bypass surgery, pipeline embolization

An intracranial aneurysm, also known as a cerebral aneurysm, is a cerebrovascular disorder characterized by a localized dilation or ballooning of a blood vessel in the brain due to a weakness in the vessel wall. These aneurysms can occur in any part of the brain but are most commonly found in the arteries of the cerebral arterial circle. The risk of rupture varies with the size and location of the aneurysm, with those in the posterior circulation being more prone to rupture.

Cerebral aneurysms are classified by size into small, large, giant, and super-giant, and by shape into saccular (berry), fusiform, and microaneurysms. Saccular aneurysms are the most common type and can result from various risk factors, including genetic conditions, hypertension, smoking, and drug abuse.

Symptoms of an unruptured aneurysm are often minimal, but a ruptured aneurysm can cause severe headaches, nausea, vision impairment, and loss of consciousness, leading to a subarachnoid hemorrhage. Treatment options include surgical clipping and endovascular coiling, both aimed at preventing further bleeding.

Diagnosis typically involves imaging techniques such as CT or MR angiography and lumbar puncture to detect subarachnoid hemorrhage. Prognosis depends on factors like the size and location of the aneurysm and the patient’s age and health, with larger aneurysms having a higher risk of rupture and poorer outcomes.

Advances in medical imaging have led to increased detection of unruptured aneurysms, prompting ongoing research into their management and the development of predictive tools for rupture risk.

## Contents

* 1 Classification
* 1.1 Berry (saccular) aneurysms
* 1.2 Fusiform aneurysms
* 1.3 Microaneurysms
* 2 Signs and symptoms
* 2.1 Subarachnoid bleed
* 2.2 Microaneurysms
* 2.3 Vasospasm
* 3 Risk factors
* 3.1 Genetic associations
* 4 Pathophysiology
* 4.1 Saccular aneurysms
* 5 Diagnosis
* 6 Treatment
* 6.1 Surgical clipping
* 6.2 Endovascular coiling
* 6.3 Cerebral bypass surgery
* 7 Prognosis
* 8 Epidemiology
* 9 Clinical trials
* 9.1 International Subarachnoid Aneurysm Trial
* 9.1.1 Study design and results
* 9.1.2 Criticism
* 9.1.3 Subsequent analysis
* 10 See also
* 11 References
* 12 External links

## Classification

Diagram of cerebral aneurysm.

Cerebral aneurysms are classified both by size and shape:

* Small aneurysms have a diameter of less than 15 mm.
* Larger aneurysms include those classified as large (15 to 25 mm), giant (25 to 50 mm) (0.98 inches to 1.97 inches), and super-giant (over 50 mm).[3]

### Berry (saccular) aneurysms

Saccular aneurysms, also known as berry aneurysms, appear as a round outpouching and are the most common form of cerebral aneurysm.[3][4] Causes include connective tissue disorders, polycystic kidney disease, arteriovenous malformations, untreated hypertension, tobacco smoking, cocaine and amphetamines, intravenous drug abuse (can cause infectious mycotic aneurysms), alcoholism, heavy caffeine intake, head trauma, and infection in the arterial wall from bacteremia, i.e. mycotic aneurysms and related disorders.[5]

### Fusiform aneurysms

Fusiform dolichoectatic aneurysms represent a widening of a segment of an artery around the entire blood vessel, rather than just arising from a side of an artery's wall. They have an estimated annual risk of rupture between 1.6 and 1.9 percent.[6][7]

### Microaneurysms

Microaneurysms, also known as Charcot–Bouchard aneurysms, typically occur in small blood vessels (less than 300 micrometre diameter), most often the lenticulostriate vessels of the basal ganglia, and are associated with chronic hypertension.[8] Charcot–Bouchard aneurysms are a common cause of intracranial hemorrhage.[9]

## Signs and symptoms

A small, unchanging aneurysm will produce few, if any, symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or no symptoms at all.[10]

### Subarachnoid bleed

If an aneurysm ruptures, blood leaks into the space around the brain. This is called a subarachnoid hemorrhage. Onset is usually sudden without prodrome, classically presenting as a "thunderclap headache" worse than previous headaches.[11][12] Symptoms of a subarachnoid hemorrhage differ depending on the site and size of the aneurysm.[12] Symptoms of a ruptured aneurysm can include:[13]

* a sudden severe headache that can last from several hours to days
* nausea and vomiting
* drowsiness, confusion and/or loss of consciousness
* visual abnormalities
* meningism
* dizziness

Almost all aneurysms rupture at their apex. This leads to hemorrhage in the subarachnoid space and sometimes in brain parenchyma. Minor leakage from aneurysm may precede rupture, causing warning headaches. About 60% of patients die immediately after rupture.[14] Larger aneurysms have a greater tendency to rupture, though most ruptured aneurysms are less than 10 mm in diameter.[12]

### Microaneurysms

A ruptured microaneurysm may cause an intracerebral hemorrhage, presenting as a focal neurological deficit.[12]

Rebleeding, hydrocephalus (the excessive accumulation of cerebrospinal fluid), vasospasm (spasm, or narrowing, of the blood vessels), or multiple aneurysms may also occur. The risk of rupture from a cerebral aneurysm varies according to the size of an aneurysm, with the risk rising as the aneurysm size increases.[15]

### Vasospasm

Vasospasm, referring to blood vessel constriction, can occur secondary to subarachnoid hemorrhage following a ruptured aneurysm. This is most likely to occur within 21 days and is seen radiologically within 60% of such patients. The vasospasm is thought to be secondary to the apoptosis of inflammatory cells such as macrophages and neutrophils that become trapped in the subarachnoid space. These cells initially invade the subarachnoid space from the circulation in order to phagocytose the hemorrhaged red blood cells. Following apoptosis, it is thought there is a massive degranulation of vasoconstrictors, including endothelins and free radicals, that cause the vasospasm.[16]

## Risk factors

Intracranial aneurysms may result from diseases acquired during life, or from genetic conditions. Hypertension, smoking, alcoholism, and obesity are associated with the development of brain aneurysms.[11][12][17] Cocaine use has also been associated with the development of intracranial aneurysms.[12]

Other acquired associations with intracranial aneurysms include head trauma and infections.[11]

### Genetic associations

Coarctation of the aorta is also a known risk factor,[11] as is arteriovenous malformation.[14] Genetic conditions associated with connective tissue disease may also be associated with the development of aneurysms.[11] This includes:[18]

* autosomal dominant polycystic kidney disease,
* neurofibromatosis type I,
* Marfan syndrome,
* multiple endocrine neoplasia type I,
* pseudoxanthoma elasticum,
* hereditary hemorrhagic telangiectasia and
* Ehlers-Danlos syndrome types II and IV.

Specific genes have also had reported association with the development of intracranial aneurysms, including perlecan, elastin, collagen type 1 A2, endothelial nitric oxide synthase, endothelin receptor A and cyclin dependent kinase inhibitor. Recently, several genetic loci have been identified as relevant to the development of intracranial aneurysms. These include 1p34–36, 2p14–15, 7q11, 11q25, and 19q13.1–13.3.[19]

## Pathophysiology

Aneurysm means an outpouching of a blood vessel wall that is filled with blood. Aneurysms occur at a point of weakness in the vessel wall. This can be because of acquired disease or hereditary factors. The repeated trauma of blood flow against the vessel wall presses against the point of weakness and causes the aneurysm to enlarge.[20] As described by the law of Young-Laplace, the increasing area increases tension against the aneurysmal walls, leading to enlargement.[21][22][23] In addition, a combination of computational fluid dynamics and morphological indices have been proposed as reliable predictors of cerebral aneurysm rupture.[24]

Both high and low wall shear stress of flowing blood can cause aneurysm and rupture. However, the mechanism of action is still unknown. It is speculated that low shear stress causes growth and rupture of large aneurysms through inflammatory response while high shear stress causes growth and rupture of small aneurysm through mural response (response from the blood vessel wall). Other risk factors that contributes to the formation of aneurysm are: cigarette smoking, hypertension, female gender, family history of cerebral aneurysm, infection, and trauma. Damage to structural integrity of the arterial wall by shear stress causes an inflammatory response with the recruitment of T cells, macrophages, and mast cells. The inflammatory mediators are: interleukin 1 beta, interleukin 6, tumor necrosis factor alpha (TNF alpha), MMP1, MMP2, MMP9, prostaglandin E2, complement system, reactive oxygen species (ROS), and angiotensin II. However, smooth muscle cells from the tunica media layer of the artery moved into the tunica intima, where the function of the smooth muscle cells changed from contractile function into pro-inflammatory function. This causes the fibrosis of the arterial wall, with reduction of number of smooth muscle cells, abnormal collagen synthesis, resulting in a thinning of the arterial wall and the formation of aneurysm and rupture. No specific gene loci has been identified to be associated with cerebral aneurysms.[25]

Generally, aneurysms larger than 7 mm in diameter should be treated because they are prone for rupture. Meanwhile, aneurysms less than 7 mm arise from the anterior and posterior communicating artery and are more easily ruptured when compared to aneurysms arising from other locations.[25]

### Saccular aneurysms

The most common sites of intracranial saccular aneurysms

Saccular aneurysms are almost always the result of hereditary weaknesses in blood vessels and typically occur within the arteries of the circle of Willis,[20][26] in order of frequency affecting the following arteries:[27]

* Anterior communicating artery
* Posterior communicating artery
* Middle cerebral artery
* Internal carotid artery
* Tip of basilar artery

Saccular aneurysms tend to have a lack of tunica media and elastic lamina around their dilated locations (congenital), with a wall of sac made up of thickened hyalinized intima and adventitia.[14] In addition, some parts of the brain vasculature are inherently weak—particularly areas along the circle of Willis, where small communicating vessels link the main cerebral vessels. These areas are particularly susceptible to saccular aneurysms.[11] Approximately 25% of patients have multiple aneurysms, predominantly when there is a familial pattern.[12]

## Diagnosis

CT angiography showing aneurysm measuring 2.6 mm in diameter at the ACOM (anterior communicating artery).

Once suspected, intracranial aneurysms can be diagnosed radiologically using magnetic resonance or CT angiography.[28] But these methods have limited sensitivity for diagnosis of small aneurysms, and often cannot be used to specifically distinguish them from infundibular dilations without performing a formal angiogram.[28][29] The determination of whether an aneurysm is ruptured is critical to diagnosis. Lumbar puncture (LP) is the gold standard technique for determining aneurysm rupture (subarachnoid hemorrhage). Once an LP is performed, the CSF is evaluated for RBC count, and presence or absence of xanthochromia.[30]

## Treatment

A selection of Mayfield and Drake aneurysm clips ready for implantation.

Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Currently there are two treatment options for securing intracranial aneurysms: surgical clipping or endovascular coiling. If possible, either surgical clipping or endovascular coiling is typically performed within the first 24 hours after bleeding to occlude the ruptured aneurysm and reduce the risk of recurrent hemorrhage.[31]

While a large meta-analysis found the outcomes and risks of surgical clipping and endovascular coiling to be statistically similar, no consensus has been reached.[32] In particular, the large randomised control trial International Subarachnoid Aneurysm Trial appears to indicate a higher rate of recurrence when intracerebral aneurysms are treated using endovascular coiling. Analysis of data from this trial has indicated a 7% lower eight-year mortality rate with coiling,[33] a high rate of aneurysm recurrence in aneurysms treated with coiling—from 28.6 to 33.6% within a year,[34][35] a 6.9 times greater rate of late retreatment for coiled aneurysms,[36] and a rate of rebleeding 8 times higher than surgically clipped aneurysms.[37]

### Surgical clipping

Aneurysms can be treated by clipping the base of the aneurysm with a specially designed clip. Whilst this is typically carried out by craniotomy, a new endoscopic endonasal approach is being trialed.[38] Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937.[39] After clipping, a catheter angiogram or CTA can be performed to confirm complete clipping.[40]

### Endovascular coiling

Main article: Medicine:Endovascular coiling

Endovascular coiling refers to the insertion of platinum coils into the aneurysm. A catheter is inserted into a blood vessel, typically the femoral artery, and passed through blood vessels into the cerebral circulation and the aneurysm. Coils are pushed into the aneurysm, or released into the blood stream ahead of the aneurysm. Upon depositing within the aneurysm, the coils expand and initiate a thrombotic reaction within the aneurysm. If successful, this prevents further bleeding from the aneurysm.[41] In the case of broad-based aneurysms, a stent may be passed first into the parent artery to serve as a scaffold for the coils.[42]

### Cerebral bypass surgery

Cerebral bypass surgery was developed in the 1960s in Switzerland by Gazi Yaşargil. When a patient has an aneurysm involving a blood vessel or a tumor at the base of the skull wrapping around a blood vessel, surgeons eliminate the problem vessel by replacing it with an artery from another part of the body.[43]

## Prognosis

Outcomes depend on the size of the aneurysm.[44] Small aneurysms (less than 7 mm) have a low risk of rupture and increase in size slowly.[44] The risk of rupture is less than one percent for aneurysms of this size.[44]

The prognosis for a ruptured cerebral aneurysm depends on the extent and location of the aneurysm, the person's age, general health, and neurological condition. Some individuals with a ruptured cerebral aneurysm die from the initial bleeding. Other individuals with cerebral aneurysm recover with little or no neurological deficit. The most significant factors in determining outcome are the Hunt and Hess grade, and age. Generally, patients with Hunt and Hess grade I and II hemorrhage on admission to the emergency room and patients who are younger within the typical age range of vulnerability can anticipate a good outcome, without death or permanent disability. Older patients and those with poorer Hunt and Hess grades on admission have a poor prognosis. Generally, about two-thirds of patients have a poor outcome, death, or permanent disability.[20][45][46]

Increased availability and greater access to medical imaging has caused a rising number of asymptomatic, unruptured cerebral aneurysms to be discovered incidentally during medical imaging investigations.[47] Unruptured aneurysms may be managed by endovascular clipping or stenting. For those subjects that underwent follow-up for the unruptured aneurysm, computed tomography angiography (CTA) or magnetic resonance angiography (MRA) of the brain can be done yearly.[48] Recently, an increasing number of aneurysm features have been evaluated in their ability to predict aneurysm rupture status, including aneurysm height, aspect ratio, height-to-width ratio, inflow angle, deviations from ideal spherical or elliptical forms, and radiomics morphological features.[49]

## Epidemiology

The prevalence of intracranial aneurysm is about 1–5% (10 million to 12 million persons in the United States) and the incidence is 1 per 10,000 persons per year in the United States (approximately 27,000), with 30- to 60-year-olds being the age group most affected.[10][20] Intracranial aneurysms occur more in women, by a ratio of 3 to 2, and are rarely seen in pediatric populations.[10][17]

## Clinical trials

### International Subarachnoid Aneurysm Trial

The International Subarachnoid Aneurysm Trial (ISAT) was a large multicenter prospective randomized clinical medical trial comparing the safety and efficacy of endovascular coil treatment and surgical clipping for the treatment of brain aneurysms. The study began in 1994 with the first results being published in The Lancet in 2002, and the 10-year data were published again in The Lancet in early September 2005. A total of 2,143 study participants were mostly drawn from U.K. hospitals, with the rest drawn from North American and European hospitals.

The study found superior results with endovascular coil treatment compared to surgical clipping. However, subsequent studies have questioned this conclusion.[50] The study was criticized by many clinicians and was not accepted by most surgeons.[51] Primary criticisms were related to the study's generalizability and the long-term prognosis of coil embolization.[52]

#### Study design and results

ISAT sought to measure outcomes of cerebral aneurysm patients at 2 and 12 months using a type of Rankin scale.[53]: 114 The study was prematurely terminated in 2002 after the oversight committee determined there was increased morbidity with surgical clipping compared to endovascular coiling.[53]: 114

#### Criticism

ISAT was criticized on several factors related to the randomization of the patient population. The randomized patient population in the ISAT was younger on average; the majority had aneurysms under 10 mm and in anterior circulation compared to the population of subarachnoid hemorrhage patients in the U.S. and Japan.[50][54]: 210 In response to these criticisms, a facility that participated in ISAT compared the clinical outcomes of their patients who were not selected for the study to those who were. They reported similar outcomes to the ISAT.[50]

#### Subsequent analysis

Although the initial ISAT analysis appeared to favor endovascular coiling over microsurgical clipping, subsequent meta-analysis have questioned that conclusion finding higher incidences[spelling?] of recurrence.[55] A large meta-analysis from Johns Hopkins University published in Neurosurgery concluded that "there is no clear consensus in these two studies or in the 45 observational studies included."[55]

Updated data from the ISAT group in March 2008 shows that the higher aneurysm rate of recurrence is also associated with a higher re-bleeding rate, given that the re-bleed rate of coiled aneurysms appears to be 8 times higher than that of aneurysms treated with surgical clipping in this study.[56] The ISAT authors conclude that "when treating ruptured cerebral aneurysms, the advantage of coil embolization over clip ligation cannot be assumed for patients younger than 40 years old."[56] Other studies have directly questioned the ISAT's conclusions.[57] This conclusion is based on a number of methodological assumptions itself and other authors have cautioned about extending it to other patient populations.[58]

## See also

* Interventional neuroradiology
* Intradural pseudoaneurysm

## References

1. ↑ 1.0 1.1 "Brain aneurysm - Symptoms and causes". https://www.mayoclinic.org/diseases-conditions/brain-aneurysm/symptoms-causes/syc-20361483.
2. ↑ "What is an Aneurysm?". https://www.webmd.com/heart-disease/understanding-aneurysm-basics.
3. ↑ 3.0 3.1 "What You Should Know About Cerebral Aneurysms". 8 August 2021. http://www.hopkinsmedicine.org/healthlibrary/conditions/nervous_system_disorders/cerebral_aneurysm_85,P08772/.
4. ↑ Bhidayasiri, Roongroj; Waters, Michael F.; Giza, Christopher C. (2005). Neurological differential diagnosis : a prioritized approach (3. Dr. ed.). Oxford: Blackwell Publishing. p. 133. ISBN 978-1-4051-2039-5. https://archive.org/details/neurologicaldiff00bhid.
5. ↑ Koutsothanasis G.A.; Sampath R., Berry Aneurysm (update: October 2, 2020). Link https://www.ncbi.nlm.nih.gov/books/NBK557480/
6. ↑ Xu, David S.; Levitt, Michael R.; Kalani, M. Yashar S.; Rangel-Castilla, Leonardo; Mulholland, Celene B.; Abecassis, Isaac J.; Morton, Ryan P.; Nerva, John D. et al. (2017-04-07). "Dolichoectatic aneurysms of the vertebrobasilar system: clinical and radiographic factors that predict poor outcomes" (in en-US). Journal of Neurosurgery 128 (2): 560–66. doi:10.3171/2016.10.JNS161041. ISSN 1933-0693. PMID 28387624. https://thejns.org/view/journals/j-neurosurg/128/2/article-p560.xml.
7. ↑ Fusiform and dolichoectatic aneurysms By James R Brorson MD (Dr. Brorson of the University of Chicago received consultation fees from CVS-Caremark, National Peer Review Corporation, and Medico-legal Consulting.) Originally released October 28, 1997; last updated January 29, 2017; expires January 29, 2020 https://tcapp.org/wp-content/uploads/2017/09/Fusiform-and-Dolichoectatic-Aneurysms.pdf
8. ↑ Kumar; Abbas; Fausto, eds (2005). Robbins and Cotran Pathologic Basis of Disease (7th ed.). China: Elsevier. ISBN 978-0-7216-0187-8.
9. ↑ Gupta, Kashvi; M Das, Joe (2021), Charcot Bouchard Aneurysm, Treasure Island (FL): StatPearls Publishing, PMID 31971704, https://www.ncbi.nlm.nih.gov/books/NBK553028/, retrieved 2021-05-06
10. ↑ 10.0 10.1 10.2 Brisman, JL; Song, JK; Newell, DW (Aug 31, 2006). "Cerebral aneurysms.". The New England Journal of Medicine 355 (9): 928–39. doi:10.1056/nejmra052760. PMID 16943405.
11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 Goljan, Edward F. (2006). Rapid Review Pathology (2nd ed.). St. Louis: Mosby. p. 158. ISBN 978-0-323-04414-1.
12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 Stroke Essentials for Primary Care: A Practical Guide. New York: Humana Press. 2009. pp. 86–88, 153. ISBN 978-1-934115-01-5. https://archive.org/details/strokeessentials00alwa_561.
13. ↑ Publishing, Harvard Health (18 December 2018). "Subarachnoid Hemorrhage". https://www.health.harvard.edu/a_to_z/subarachnoid-hemorrhage-a-to-z.
14. ↑ 14.0 14.1 14.2 DiMaio, Vincent J.; DiMaio, Dominick (2001). Forensic pathology (2nd ed.). Boca Raton, FL: CRC Press. p. 61. ISBN 978-0-8493-0072-1. https://archive.org/details/forensicpatholog0000dima/page/61.
15. ↑ Korja Miikka; Lehto Hanna; Juvela Seppo (2014-07-01). "Lifelong Rupture Risk of Intracranial Aneurysms Depends on Risk Factors". Stroke 45 (7): 1958–63. doi:10.1161/STROKEAHA.114.005318. PMID 24851875.
16. ↑ Gallia, Gary L.; Tamargo, Rafael J. (1 October 2006). "Leukocyte-endothelial cell interactions in chronic vasospasm after subarachnoid hemorrhage". Neurological Research 28 (7): 750–58. doi:10.1179/016164106X152025. PMID 17164038.
17. ↑ 17.0 17.1 Brown, Walter L. Kemp, Dennis K. Burns, Travis G. (2008). Pathology the big picture. New York: McGraw-Hill Medical. p. 148. ISBN 978-0-07-159379-3.
18. ↑ Caranci, F.; Briganti, F.; Cirillo, L.; Leonardi, M.; Muto, M. (2012). "Epidemiology and genetics of intracranial aneurysms". European Journal of Radiology 82 (10): 1598–605. doi:10.1016/j.ejrad.2012.12.026. PMID 23399038.
19. ↑ van der Voet, M; Olson, J; Kuivaniemi, H; Dudek, D; Skunca, M; Ronkainen, A; Niemelä, M; Jääskeläinen, J et al. (1 March 2004). "Intracranial Aneurysms in Finnish Families: Confirmation of Linkage and Refinement of the Interval to Chromosome 19q13.3". The American Journal of Human Genetics 74 (3): 564–71. doi:10.1086/382285. PMID 14872410.
20. ↑ 20.0 20.1 20.2 20.3 Haberland, Catherine (2007). Clinical neuropathology : text and color atlas (Online-Ausg. ed.). New York: Demos. p. 70. ISBN 978-1-888799-97-2. https://archive.org/details/clinicalneuropat00habe_423.
21. ↑ Humphrey, J. D.; Kyriacou, S. K. (June 1996). "The use of Laplace's equation in aneurysm mechanics". Neurological Research 18 (3): 204–08. doi:10.1080/01616412.1996.11740404. ISSN 0161-6412. PMID 8837052.
22. ↑ "Laplace's Law and Aneurysms" (in en). https://sciencedemonstrations.fas.harvard.edu/presentations/laplaces-law-and-aneurysms.
23. ↑ Hademenos, George J. (2008-01-11). "The Physics of Cerebral Aneurysms" (in en). Physics Today 48 (2): 24. doi:10.1063/1.881442. ISSN 0031-9228. https://physicstoday.scitation.org/doi/abs/10.1063/1.881442.
24. ↑ Amigo, Nicolás; Valencia, Alvaro; Wu, Wei; Patnaik, Sourav; Finol, Ender (2021-03-08). "Cerebral aneurysm rupture status classification using statistical and machine learning methods". Proceedings of the Institution of Mechanical Engineers, Part H 235 (6): 655–662. doi:10.1177/09544119211000477. ISSN 2041-3033. PMID 33685288.
25. ↑ 25.0 25.1 Chalouhi, Nohra; Loh, Brian L; Hasan, David (25 November 2013). "Review of Cerebral Aneurysm Formation, Growth, and Rupture". Stroke 44 (12): 3613–22. doi:10.1161/STROKEAHA.113.002390. PMID 24130141.
26. ↑ "berry aneurysm" at Dorland's Medical Dictionary
27. ↑ Howlett, David; Ayers, Brian (2004). The hands-on guide to imaging. Oxford: Blackwell. p. 204. ISBN 978-1-4051-1551-3. https://archive.org/details/handsonguidetoim00howl.
28. ↑ 28.0 28.1 White, Philip M.; Teasdale, Evelyn M.; Wardlaw, Joanna M.; Easton, Valerie (2001-06-01). "Intracranial Aneurysms: CT Angiography and MR Angiography for Detection – Prospective Blinded Comparison in a Large Patient Cohort". Radiology 219 (3): 739–49. doi:10.1148/radiology.219.3.r01ma16739. ISSN 0033-8419. PMID 11376263.
29. ↑ Greenberg, Mark (2010). Handbook of neurosurgery. Greenberg Graphics. ISBN 978-1-60406-326-4. OCLC 892183792.
30. ↑ Mark, Dustin G.; Kene, Mamata V.; Offerman, Steven R.; Vinson, David R.; Ballard, Dustin W. (2015). "Validation of cerebrospinal fluid findings in aneurysmal subarachnoid hemorrhage". The American Journal of Emergency Medicine 33 (9): 1249–52. doi:10.1016/j.ajem.2015.05.012. PMID 26022754.
31. ↑ Park, Jaechan; Woo, Hyunjin; Kang, Dong-Hun; Kim, Yong-Sun; Kim, Min Young; Shin, Im Hee; Kwak, Sang Gyu (2015-02-01). "Formal protocol for emergency treatment of ruptured intracranial aneurysms to reduce in-hospital rebleeding and improve clinical outcomes" (in en-US). Journal of Neurosurgery 122 (2): 383–91. doi:10.3171/2014.9.JNS131784. ISSN 1933-0693. PMID 25403841. https://thejns.org/view/journals/j-neurosurg/122/2/article-p383.xml.
32. ↑ Raja, PV; Huang, J; Germanwala, AV; Gailloud, P; Murphy, KP; Tamargo, RJ (June 2008). "Microsurgical clipping and endovascular coiling of intracranial aneurysms: a critical review of the literature.". Neurosurgery 62 (6): 1187–202; discussion 1202–03. doi:10.1227/01.neu.0000333291.67362.0b. PMID 18824986.
33. ↑ Mitchell P, Kerr R, Mendelow AD, Molyneux A. "Could late rebleeding overturn the superiority of cranial aneurysm coil embolization over clip ligation seen in ISAT?" Journal of Neurosurgery 108: 437–42, March 2008
34. ↑ Piotin, M; Spelle, L; Mounayer, C; Salles-Rezende, MT; Giansante-Abud, D; Vanzin-Santos, R; Moret, J (May 2007). "Intracranial aneurysms: treatment with bare platinum coils – aneurysm packing, complex coils, and angiographic recurrence". Radiology 243 (2): 500–08. doi:10.1148/radiol.2431060006. PMID 17293572.
35. ↑ Raymond, J; Guilbert, F; Weill, A; Georganos, SA; Juravsky, L; Lambert, A; Lamoureux, J; Chagnon, M et al. (June 2003). "Long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils". Stroke 34 (6): 1398–1403. doi:10.1161/01.STR.0000073841.88563.E9. PMID 12775880.
36. ↑ "Retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT)". Stroke 38 (5): 1538–44. May 2007. doi:10.1161/STROKEAHA.106.466987. PMID 17395870.
37. ↑ "Could late rebleeding overturn the superiority of cranial aneurysm coil embolization over clip ligation seen in the International Subarachnoid Aneurysm Trial?". J. Neurosurg. 108 (3): 437–42. March 2008. doi:10.3171/JNS/2008/108/3/0437. PMID 18312088.
38. ↑ "Germanwala Presents First Aneurysm Patient Treated Through Nose". June 25, 2009. https://www.med.unc.edu/surgery/germanwala-presents-first-aneurysm-patient-treated-through-nose/.
39. ↑ Sasidharan, Gopalakrishnan Madhavan; Sastri, Savitr B V; Pandey, Paritosh (1 January 2015). "Aneurysm clips: What every resident should know". Neurology India 63 (1). https://www.neurologyindia.com/text.asp?2015/63/1/96/152666.
40. ↑ Bharatha A, Yeung R, Durant D, Fox AJ, Aviv RI, Howard P, Thompson AL, Bartlett ES, Symons SP. "Comparison of computed tomography angiography with digital subtraction angiography in the assessment of clipped intracranial aneurysms". Journal of Computer Assisted Tomography. 2010 May–June; 34(3): 440–45.
41. ↑ "Treatment of intracranial aneurysms by embolization with coils: a systematic review". Stroke 30 (2): 470–76. February 1999. doi:10.1161/01.STR.30.2.470. PMID 9933290.
42. ↑ Oushy, Soliman; Rinaldo, Lorenzo; Brinjikji, Waleed; Cloft, Harry; Lanzino, Giuseppe (June 2020). "Recent advances in stent-assisted coiling of cerebral aneurysms". Expert Review of Medical Devices 17 (6): 519–32. doi:10.1080/17434440.2020.1778463. ISSN 1745-2422. PMID 32500761.
43. ↑ Spetzler, Robert; Chater, Norman (1 November 1976). "Microvascular bypass surgery". Journal of Neurosurgery 45 (5): 508–13. doi:10.3171/jns.1976.45.5.0508. PMID 972334.
44. ↑ 44.0 44.1 44.2 "Growth and Rupture Risk of Small Unruptured Intracranial Aneurysms: A Systematic Review". Ann. Intern. Med. 167 (1): 26–33. July 2017. doi:10.7326/M17-0246. PMID 28586893.
45. ↑ Hop, J. W.; Rinkel, G. J.E.; Algra, A.; van Gijn, J. (1 March 1997). "Case-Fatality Rates and Functional Outcome After Subarachnoid Hemorrhage : A Systematic Review". Stroke 28 (3): 660–64. doi:10.1161/01.STR.28.3.660. PMID 9056628.
46. ↑ Ljunggren, B; Sonesson, B; Säveland, H; Brandt, L (May 1985). "Cognitive impairment and adjustment in patients without neurological deficits after aneurysmal SAH and early operation.". Journal of Neurosurgery 62 (5): 673–79. doi:10.3171/jns.1985.62.5.0673. PMID 3989590.
47. ↑ Vernooij, MW; Ikram, MA; Tanghe, HL (2007). "Incidental findings on brain MRI in the general population.Incidental findings on brain MRI in the general population.". N Engl J Med 357 (5): 1821–28. doi:10.1056/NEJMoa070972. PMID 17978290.
48. ↑ Thompson, B. Gregory; Brown, Robert D.; Amin-Hanjani, Sepideh; Broderick, Joseph P.; Cockroft, Kevin M.; Connolly, E. Sander; Duckwiler, Gary R.; Harris, Catherine C. et al. (August 2015). "Guidelines for the Management of Patients With Unruptured Intracranial Aneurysms: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association" (in en). Stroke 46 (8): 2368–2400. doi:10.1161/STR.0000000000000070. ISSN 0039-2499. PMID 26089327.
49. ↑ Ludwig, CG; Lauric, A; Malek, JA; Mulligan, R; Malek, AM (2020). "Performance of Radiomics derived morphological features for prediction of aneurysm rupture status.". Journal of NeuroInterventional Surgery 13 (8). doi:10.1136/neurintsurg-2020-016808. PMID 33158993.
50. ↑ 50.0 50.1 50.2 AJNR Am J Neuroradiol. 2005 Feb;26(2):367-72.
51. ↑ Michael Forsting, Isabel Wanke, Intracranial Vascular Malformations and Aneurysms: From Diagnostic Work-Up to Endovascular Therapy, Springer 2008, ISBN 3-540-32919-6.
52. ↑ Michael J. Alexander, Robert Friedrich Spetzler, Pediatric neurovascular disease: surgical, endovascular, and medical management, Thieme: 2006, ISBN 1-58890-368-0, page 145.
53. ↑ 53.0 53.1 Michael S. Horowitz, Elad I. Levy, Neuroendovascular surgery, Karger Publishers, 2005, ISBN 3-8055-7781-8.
54. ↑ Adnan I. Qureshi, Textbook of Interventional Neurology, Ed. Adnan I. Qureshi, Alexandros L. Georgiadis, Cambridge University Press: 2011, ISBN 0-521-87639-7.
55. ↑ 55.0 55.1 See, Raja PV, Huang J, Germanwala AV, Gailloud P, Murphy KP, Tamargo RJ. Microsurgical clipping and endovascular coiling of intracranial aneurysms: A critical review of the literature. Neurosurgery 62: 1187-1202, June 2008
56. ↑ 56.0 56.1 Mitchell P, Kerr R, Mendelow AD, Molyneux A. Could late rebleeding overturn the superiority of cranial aneurysm coil embolization over clip ligation seen in ISAT? Journal of Neurosurgery 108: 437-442, March 2008
57. ↑ See, J Neurosurg. 2010 Oct;113(4):795-801.
58. ↑ J Mocco, L. Nelson Hopkins, "International Subarachnoid Aneurysm Trial analysis", Journal of Neurosurgery, March 2008 / Vol. 108 / No. 3 / Pages 436-436.

## External links

* National Institute of Neurological Disorders and Stroke

Classification|

* ICD-11: 8B22.5
* ICD-10: I67.1
* ICD-9-CM: 437.3
* MeSH: D002532
* SNOMED CT: 128609009

|

External resources|

* MedlinePlus: 001414

* v
* t
* e

Cerebrovascular diseases

Brain ischemia/
cerebral infarction
(ischemic stroke/TIA)|

| TACI, PACI|

* precerebral: Carotid artery stenosis

* cerebral: MCA
* ACA
* Amaurosis fugax

* Moyamoya disease

|

POCI|

* precerebral: Anterior spinal artery syndrome
* Vertebrobasilar insufficiency
* Subclavian steal syndrome

* brainstem: medulla
* Medial medullary syndrome
* Lateral medullary syndrome
* pons
* Medial pontine syndrome/Foville's
* Lateral pontine syndrome/Millard-Gubler
* midbrain
* Weber's
* Benedikt
* Claude's

* cerebral: PCA
* Lacunar stroke
* Dejerine–Roussy syndrome

* cerebellar

General|

* cerebral: Cerebral venous sinus thrombosis
* CADASIL
* Binswanger's disease
* Transient global amnesia

Intracranial hemorrhage
(hemorrhagic stroke)|

| Extra-axial|

* Epidural
* Subdural
* Subarachnoid

|

Cerebral/Intra-axial|

* Intraventricular

Brainstem|

* Duret haemorrhages

Aneurysm|

* Cerebral aneurysm
* Intracranial berry aneurysm
* Charcot–Bouchard aneurysm

Other/general|

* Cerebral vasculitis

* v
* t
* e

Cardiovascular disease (vessels) (I70–I99, 440–456)

Arteries, arterioles
and capillaries|

| Inflammation|

* Arteritis
* Aortitis
* Buerger's disease

|

Peripheral artery disease|

| Arteriosclerosis|

* Atherosclerosis
* Foam cell
* Fatty streak
* Atheroma
* Intermittent claudication
* Critical limb ischemia

* Monckeberg's arteriosclerosis
* Arteriolosclerosis
* Hyaline
* Hyperplastic
* Cholesterol
* LDL
* Oxycholesterol
* Trans fat

|

Stenosis|

* Carotid artery stenosis
* Renal artery stenosis

Other|

* Aortoiliac occlusive disease
* Degos disease
* Erythromelalgia
* Fibromuscular dysplasia
* Raynaud's phenomenon

Aneurysm / dissection /
pseudoaneurysm|

* torso: Aortic aneurysm
* Abdominal aortic aneurysm
* Thoracic aortic aneurysm
* Aneurysm of sinus of Valsalva
* Aortic dissection
* Aortic rupture
* Coronary artery aneurysm
* head / neck
* Intracranial aneurysm
* Intracranial berry aneurysm
* Carotid artery dissection
* Vertebral artery dissection
* Familial aortic dissection

Vascular malformation|

* Arteriovenous fistula
* Arteriovenous malformation
* Telangiectasia
* Hereditary hemorrhagic telangiectasia

Vascular nevus|

* Cherry hemangioma
* Halo nevus
* Spider angioma

Veins|

| Inflammation|

* Phlebitis

|

Venous thrombosis /
Thrombophlebitis|

* primarily lower limb
* Deep vein thrombosis
* abdomen
* Hepatic veno-occlusive disease
* Budd–Chiari syndrome
* May–Thurner syndrome
* Portal vein thrombosis
* Renal vein thrombosis
* upper limb / torso
* Mondor's disease
* Paget–Schroetter disease
* head
* Cerebral venous sinus thrombosis
* Post-thrombotic syndrome

Varicose veins|

* Gastric varices
* Portacaval anastomosis
* Caput medusae
* Esophageal varices
* Hemorrhoid
* Varicocele

Other|

* Chronic venous insufficiency
* Chronic cerebrospinal venous insufficiency
* Superior vena cava syndrome
* Inferior vena cava syndrome
* Venous ulcer

Arteries or veins|

* Angiopathy
* Macroangiopathy
* Microangiopathy
* Embolism
* Pulmonary embolism
* Cholesterol embolism
* Paradoxical embolism
* Thrombosis
* Vasculitis

Blood pressure|

| Hypertension|

* Hypertensive heart disease
* Hypertensive emergency
* Hypertensive nephropathy
* Essential hypertension
* Secondary hypertension
* Renovascular hypertension
* Benign hypertension
* Pulmonary hypertension
* Systolic hypertension
* White coat hypertension

|

Hypotension|

* Orthostatic hypotension

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