The acquired factors include smoking, hypertension, traumatic brain injury, and sepsis. Although acquired factors are not as strongly associated with IA’s, they affect many IA cases and are potentially more manageable. Management of these patients consists of prevention, patient screening, and prophylactic aneurysm repair (Pfohman and Criddle, Epidemiology of intracranial aneurysm and subarachnoid hemorrhage. Journal of Neuroscience Nursing 33:39-41,2001).
Epidemiologic studies have identified certain risk factors associated with brain or intracranial aneurysms (IA). The genetic factors include a family history and the presence of certain heritable tissue disorders such as Ehlers-Danlos syndrome, Marfan's syndrome, neurogibromatosis, and polycystic kidney disease. Only about 5% of all IA cases are associated with hertiable connective tissue disorders, which cause blood vessel wall defects in various ways.
This is the most important risk factor. There is a 2- to 7-fold increased risk of intracranial aneurysm (IA) formation and subarachnoid aneurismal hemorrhage (SAH) in first-degree relatives (parents, children, and siblings).
Familial intracranial aneurysms account for 7-20% of patients with aneurismal subarachnoid hemorrhage (ASAH), but are generally not associated with any heritable tissue disorders. First-degree relatives of patients with ASAH have a four-fold risk of ruptured intracranial aneurysm compared to the general population (Shievink, Genetics of intracranial aneurysms. Neurosurgery 40(4): 651-663,1998). Another study found a 2 to 7-fold increased risk with familial relatives (Pfohman, 2001). However, a commonly quoted statistic in the literature is up to 10% in certain populations can be familial (Astradsson and Astrup, An intracranial aneurysm in one identical twin, but no aneurysm in the other, Br J Neurosurg. 2001 Apr;15(2):168-71).
The highest familial association is among siblings, 52% (Astradsson, 2001; Adams, 1992). Familial aneurysms tend to rupture at a younger age (avg. 39.8 yrs), smaller size and less frequently in the anterior communicating artery than sporadic aneurysms in the general population. In siblings and twins, they tend to occur in the same or opposite vessels and rupture also at similar ages. One study shows a trend of intracranial aneurysms as having a male/female ratio of 2/1 in all patients, 3/1 for occurrence of the intracranial aneurysm in patients under 20 yrs. However, this ratio reverses itself with female predominance in patients over 60 yrs (1/2) (Adams, 1992).
Investigations for genetic markers have been performed, but none have been successful in isolating a gene that appears to be mutating coincidental to aneurismal formation or even to the weakening of vessel walls. Ostergaard et al. investigated the occurrence of the C3-F gene among patients with IA suggesting that this gene which has been associated with atherosclerotic vascular diseases may be a risk factor for early aneurysm rupture (Puchner, 1994) and a Mendelian inheritance has been postulated (Astradsson, 2001). However, in spite of these genetic studies, the pattern of inheritance for familial aneurysms (if there is one) remains unproven.
Because of the morbidity (damage to brain function) and mortality rates associated with surgical intervention, screening for aneurysms remains controversial. One paper suggests that two groups of patients may benefit from early detection: those with autosomal dominant polycystic kidney disease and those with a history of aneurysmal subarachnoid hemorrhage (Vega et al., 2002). Vega et al. recommends that these patients undergo magnetic resonance angiography (MRI), followed by neurosurgical referral if an aneurysm is detected.
Screening of patients who have two or more family members with intracranial aneurysms is also controversial. Screening of patients who have one first-degree relative with an aneurysm does not appear to be beneficial, according to Vega et al., 2002.
Joint hypermobility (loose joints), fragile skin, easy bruising, and scarring characterize Ehlers-Danlos Type IV. There are five types with type IV being the most common and lethal (1 in 50,000-500,000 individuals). This results from a deficiency in type III collagen, which is a building block of artery and vein walls. Although the association between Ehlers-Danlos type IV and IA’s is well established, the frequency of patients with both Ehlers-Danlos and IA’s is not known due to the difficulty in diagnosing Ehlers-Danlos (a mild case involves only fragile skin and slight joint looseness). Aneurysms associated with this condition tend to form on medium to large arteries.
This syndrome is characterized by elongation of the bones and abnormalities in the cardiovascular system (the heart and blood vessels) and the eyes. It is caused by a mutation in a gene that codes for a protein component of microfibrils, used to make blood vessel walls flexible. About 1 in 10,000 to 20,000 people have this disorder. Aneurysms associated with this disorder tend to be saccular, fusiform, or dissecting and are usually found in the proximal intracranial carotid artery.
This condition begins at birth and gets progressively worse, effecting 1 in every 3,000-5,000 persons. The characteristics include blood vessel constriction (stenosis), vessel rupture, tumors in the nervous system (neurofibromas) and the abnormal development of the muscles, bones and internal organs. The aneurysms in this case tend to form in medium to large-sized arteries.
This is one of the more common heritable tissue disorders (1 in 400 to 1,000 persons). The characteristics of this disease include: enlarged kidneys, cysts in the kidneys, liver, pancreas, and spleen, cobweb-like cysts in the brain, and hernias in the groin (a vessel bulging out of the skin usually painfully). The formation of the cysts, little sacs of fluid attached to an organ, results from a genetic mutation causing abnormal cell growth and fluid secretion. Hypertension is a complication found in 75% of ADPKD patients, contributing to aneurysm formation and subarachnoid aneurismal hemorrhage in those patients.
Many studies indicate a likelihood of a relationship between ADPKD and IA’s. Estimates of the frequency of aneurysms in ADPKD patients range from 10% to 41%. IA’s have been reported in 25% of ADPKD patients and are the cause of death in 20%. Family history is an increasingly recognized risk factor for IA and SAH with ADPKD patients; about 18% to 22% of ADPKD patients with an IA have a positive family history for aneurysms.
The acquired factors including smoking, hypertension, traumatic brain injury, and sepsis. Although acquired factors are not as strongly associated with IA's, they affect many IA cases and are potentially more manageable. Management of those cases consists of prevention, patient screening, and prophylactic aneurysm repair (Pfohman and Criddle, Epidemiology of intracranial aneurysm and subarachnoid hemorrhage. Journal of Neuroscience Nursing 33:39-41,2001).
This factor accounts for less than 1% of all intracranial aneurysm (IA) cases. These aneurysms occur when an artery wall is torn due to injury, resulting in a clot formation. Although the incidence of aneurysm formation associated with TBI is small, it must be considered a risk for trauma patients for several months post-injury, especially with a head or mid-lower face injury.
This occurs when a piece of fat, bone or a nitrogen bubble (emboli) travels through the blood stream, depositing organisms that stick to the vessel wall, causing inflammation and cell death. These aneurysms account for 2-6% of IA’s and are associated usually with infections of the heart valves or pulmonary veins. They can be treated both medically and surgically, but carry a high risk of death.
While the relative incidence of traumatic brain injury and sepsis-caused aneurysms and subarachnoid aneurismal hemorrhage (SAH) are low, smoking and hypertension represent a much greater threat. Smoking is a substantial risk to both IA and SAH. It is correlated with younger age of SAH onset by 5-10 yrs, increased vasospasm (clinically confirmed constriction of the arterial vessel walls), and the development of hypertension. This leads to the reported spontaneous aneurismal SAH risk for smokers as being twice that of nonsmokers. There appears to be a relationship between IA & SAH and hypertension. The American Heart Association reports one study showing the frequency of hypertension to be 8.3 times higher among SAH patients as compared to a control group.
Studies identify several other factors contributing to IA and SAH to various degrees-age, gender, alcohol use, seasonal variations, and atherosclerosis among others. Nakagawa et al. found increasing IA with increasing age and female gender. Drinking 150 grams of alcohol or more per week has been associated with SAH. Several studies have associated atherosclerosis with IA’s and SAH. Some studies have even pointed to weather changes and atmospheric pressure as potential risk factors. More investigation is required to confirm the association of these factors.
Contributing Health Issues
At this point, the only preventative measures are screening, controlling high blood pressure and eliminating smoking. Both high blood pressure and smoking are doubly dangerous, as they contribute to a wide range of diseases, not just aneurysms. High blood pressure can affect the heart, kidneys, eyes and circulatory (blood) system.
For women, use of oral contraceptives and pregnancy can cause high blood pressure, However, 9 out of 10 of the 50 million Americans who suffer from it have no identifiable cause for their hypertension. There is no way of determining if you have high blood pressure other having your blood pressure checked by a medical professional. These are the factors that increase your susceptibility to high blood pressure:
Factors you can’t control:
Factors you can control:
A secondary type of hypertension can be caused by:
The following are recommended actions based on the "Medcohealth" website:
|Blood Pressure||Assessment||Recommended Action|
|Less than 120/80||Optimal||Recheck every two years|
|Less than 130/85||Optimal||Recheck every two years|
|130-139/85-89||High/Normal||Lifestyle changes/recheck in one year|
|140-159/90-99||Stage 1 Hypertension||Confirm in two months. Begin lifestyle changes. Get regular medical evaluations.|
|160-179/100-109||Stage 2 Hypertension||Medical evaluation. Start treatment within short period of time but no more than two months|
|180/110 or higher||Stage 3 Hypertension||Medical evaluation. Start treatment quickly but no longer than one week.|
There are ways of keeping your blood pressure under control:
De Novo formation means that the patient had a subarachnoid aneurismal hemorrhage (SAH), and was re-admitted later for another aneurysm, which was not visible during the first operation.
The Study of De Novo Aneurysms
The following information was taken from a review article (Tonn et al.,Neuroradiology 41: 674-679, 1999) of all the angiographically proven de novo cases published up to 1999 (50 patients).
The average rate of onset of symptoms of a de novo aneurysm after the first SAH is 9.9 ± 6.7yrs (range 3-34 yrs), however, 44% of these de novo aneurysms become symptomatic 3-6 years after the first SAH. Neither smoking nor patient age affected this interval, however the interval was significantly reduced for patients with a history of hypertension (6.9 ± 5.1 yrs) compared to those without (11.0 ± 3.8 yrs).
This study, in reviewing the literature, found that the likelihood of first-time congenital aneurismal SAH is 3.7-5.7 times higher for smokers. The study did not find a significant difference between ‘usual’ and de novo aneurysm formation among smokers. Smoking was more frequent with both de novo and ‘usual’ aneurysm patients than in the controls without SAH indicating that smoking contributes to both.
The study found rates of hypertension to range 25%-31% for ‘usual’ aneurysms and 67% for de novo suggesting that maintaining a low blood pressure would be useful for patients who have undergone one SAH. Smoking and arterial hypertension appear to be independent risk factors.
There is also a high risk of multiplicity in de novo formation. Most studies of de novo aneurysms show a few common clinical characteristics among patients: a history of smoking, arterial hypertension and youth. Even if these are not the actual cause of aneurysm development, they certainly aggravate the situation and encourage further development.
A certain "at-risk" group for de novo aneurysms emerges from their conclusions: "patients with a history of previous aneurismal SAH, aged 50 years or less, with arterial hypertension and a history of smoking." Apart from monitoring and treating the high blood pressure and hypertension state, the patients should refrain from smoking. They also advise follow-up angiography at an interval of 4-5 years after the initial SAH, 3 years in hypertensive patients. Note: MRA, suggested for patients with carotid ligation, may not show de novo aneurysms within the Circle of Willis.