Intracranial aneurysm

Cerebral aneurysm

Aneurysm of the basilar artery, and the vertebral arteries.
Classification and external resources
Specialty cardiology
ICD-10 I67.1
ICD-9-CM 437.3
MedlinePlus 001414
MeSH D002532

An intracranial aneurysm (also called cerebral or brain aneurysm) is a cerebrovascular disorder in which weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel.

Aneurysms in the posterior circulation (basilar artery, vertebral arteries and posterior communicating artery) have a higher risk of rupture. Basilar artery aneurysms represent only 3%-5% of all intracranial aneurysms but are the most common aneurysms in the posterior circulation.

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), and super-giant (over 50 mm).[1]

Saccular aneurysms

Saccular aneurysms, also known as berry aneurysms, appear as a round outpouching and are the most common form of cerebral aneurysm.[1][2]

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 can rupture but usually do not.

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.[3] Charcot–Bouchard aneurysms are a common cause of intracranial hemorrhage.

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 the individual may be asymptomatic (i.e., experiencing no symptoms at all).[4]

Subarachnoid haemorrhage

If an aneurysm ruptures, blood leaks into the space around the brain. This is called a subarachnoid hemorrhage. Onset is usually sudden with no prodrome, classically presenting as a "thunderclap headache" worse than previous headaches.[5][6] Symptoms of a subarachnoid hemorrhage differ depending on the site and size of the aneurysm.[6] Symptoms of a ruptured aneurysm can include:

The risk of a subarachnoid hemorrhage is greater with a saccular aneurysm than a fusiform aneurysm.

Microaneurysms

A ruptured microaneurysm may cause an intracerebral hemorrhage, presenting as a focal neurological deficit.[6]

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.

Risk factors

Intracranial aneurysms may result from diseases acquired during life, or from genetic conditions. Lifestyle diseases including hypertension, smoking, excess alcohol consumption, and obesity are associated with the development of aneurysms.[5][6][7] Cocaine use has also been associated with the development of intracranial aneurysms.[6]

Other acquired associations with intracranial aneurysms include head trauma and infections.[5]

Genetic associations

Coarctation of the aorta is also a known risk factor,[5] as is arteriovenous malformation.[8] Genetic conditions associated with connective tissue disease may also be associated with the development of aneurysms.[5] This includes:[9]

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. Mutations in interleukin 6 may be protective. . 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.[10]

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.[11] As described by the Law of Young-Laplace, the increasing area increases tension against the aneurysmal walls, leading to enlargement.

Saccular aneurysms

The most common sites of intracranial saccular aneurysms.

Saccular aneurysms are almost always the result of hereditary weakness in blood vessels and typically occur within the arteries of the Circle of Willis,[11][12] in order of frequency affecting the following arteries:[13]

Saccular aneurysms tend to have a lack of tunica media and elastic lamina around its dilated location (congenital), with wall of sac made up of thickened hyalinized intima and adventitia.[8] 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.[5] Approximately 25% of patients have multiple aneurysms, predominantly when there is familial pattern.[6]

Complications

Rupture

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.[8] Larger aneurysms have a greater tendency to rupture, though most ruptured aneurysms are less than 10 mm in diameter.[6]

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.[14]

Diagnosis

Once suspected, intracranial aneurysms can be diagnosed using angiography, magnetic resonance imaging, CT scans, and cerebrospinal fluid (CSF) analysis.

Most cerebral aneurysms are unobserved until they have already ruptured. Diagnostic tests can be used to detect if an aneurysm has or will rupture. Tests are usually required after a subarachnoid hemorrhage, to confirm the presence of an aneurysm. CSF usually shows presence of blood.

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 usually performed within the first 24 hours after bleeding to occlude the ruptured aneurysm and reduce the risk of rebleeding.

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.[15] 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,[16] a high rate of aneurysm recurrence in aneurysms treated with coiling—from 28.6-33.6% within a year,[17][18] a 6.9 times greater rate of late retreatment for coiled aneurysms,[19] and a rate of rebleeding 8 times higher than surgically-clipped aneurysms.[20]

Surgical clipping

Main article: 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 trialled.[21] Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937 [22] After clipping, a catheter angiogram or CTA can be performed to confirm complete clipping.[23]

Endovascular coiling

Main article: 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.[24] 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.

Cerebral bypass surgery

Cerebral bypass surgery was developed in the 1960s in Switzerland by Gazi Yasargil, M.D. 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.[25]

Prognosis

The prognosis for a patient with 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.[11][26][27]

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 incidence highest in 30- to 60-year-olds.[4][11] Intracranial aneurysms occur more in women, by a ratio of 3 to 2, and are rarely seen in pediatric populations.[4][7]

See also

References

  1. 1 2 http://www.hopkinsmedicine.org/healthlibrary/conditions/nervous_system_disorders/cerebral_aneurysm_85,P08772/
  2. ↑ 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.
  3. ↑ Kumar; Abbas; Fausto, eds. (2005). Robbins and Cotran Pathologic Basis of Disease (7th ed.). China: Elsevier. ISBN 0-7216-0187-1.
  4. 1 2 3 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.
  5. 1 2 3 4 5 6 Goljan, Edward F. (2006). Rapid Review Pathology (2nd ed.). St. Louis: Mosby. p. 158. ISBN 0-323-04414-X.
  6. 1 2 3 4 5 6 7 Alway, David; Cole, John Walden, eds. (2009). Stroke Essentials for Primary Care: A Practical Guide. New York: Humana Press. pp. 86–88,153. ISBN 978-1-934115-01-5.
  7. 1 2 Brown, Walter L. Kemp, Dennis K. Burns, Travis G. (2008). Pathology the big picture. New York: McGraw-Hill Medical. p. 148. ISBN 0-07-159379-9.
  8. 1 2 3 DiMaio, Vincent J.; DiMaio, Dominick (2001). Forensic pathology (2nd ed.). Boca Raton, FL [etc.]: CRC Press. p. 61. ISBN 0-8493-0072-X.
  9. ↑ 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.
  10. ↑ VANDERVOET, M; OLSON, J; KUIVANIEMI, H; DUDEK, D; SKUNCA, M; RONKAINEN, A; NIEMELA, M; JAASKELAINEN, J; HERNESNIEMI, J; HELIN, K (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): 564–571. doi:10.1086/382285.
  11. 1 2 3 4 Haberland, Catherine (2007). Clinical neuropathology : text and color atlas ([Online-Ausg.]. ed.). New York: Demos. p. 70. ISBN 978-1-888799-97-2.
  12. ↑ "berry aneurysm" at Dorland's Medical Dictionary
  13. ↑ Howlett, David; Ayers, Brian (2004). The hands-on guide to imaging. Oxford: Blackwell. p. 204. ISBN 1-4051-1551-3.
  14. ↑ Gallia, Gary L.; Tamargo, Rafael J. (1 October 2006). "Leukocyte-endothelial cell interactions in chronic vasospasm after subarachnoid hemorrhage". Neurological Research 28 (7): 750–758. doi:10.1179/016164106X152025. PMID 17164038.
  15. ↑ 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 1202–3. doi:10.1227/01.neu.0000333291.67362.0b. PMID 18824986.
  16. ↑ 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
  17. ↑ 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): 500–8. doi:10.1148/radiol.2431060006. PMID 17293572.
  18. ↑ Raymond, J; Guilbert, F; Weill, A; Georganos, SA; Juravsky, L; Lambert, A; Lamoureux, J; Chagnon, M; Roy, D (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.
  19. ↑ Campi, A; Ramzi N, Molyneaux AJ, Summers, PE, Kerr, RS, Sneade, M, Yarnold, JA, Rischmiller, J, Byrne, JV (May 2007). "Retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT)". Stroke 38 (5): 1538–44. doi:10.1161/STROKEAHA.106.466987. PMID 17395870.
  20. ↑ Mitchell P, Kerr R, Mendelow AD, Molyneux A; Kerr; Mendelow; Molyneux (March 2008). "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. doi:10.3171/JNS/2008/108/3/0437. PMID 18312088.
  21. ↑ http://www.med.unc.edu/neurosurgery/news/2010-news/germanwala-presents-first-aneurysm-patient-treated-through-nose/
  22. ↑ http://www.neurologyindia.com/text.asp?2015/63/1/96/152666
  23. ↑ 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):440-445.
  24. ↑ Brilstra, E. H.; Rinkel, G. J. E.; van der Graaf, Y.; van Rooij, W. J. J.; Algra, A. (1 February 1999). "Treatment of Intracranial Aneurysms by Embolization with Coils : A Systematic Review". Stroke 30 (2): 470–476. doi:10.1161/01.STR.30.2.470. PMID 9933290.
  25. ↑ http://thejns.org/doi/abs/10.3171/jns.1976.45.5.0508
  26. ↑ 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): 660–664. doi:10.1161/01.STR.28.3.660. PMID 9056628.
  27. ↑ 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): 673–9. doi:10.3171/jns.1985.62.5.0673. PMID 3989590.

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