The majority of CA is small and does not provoke any symptoms until rupture. Such vascular anomalies may be detected if neuroimaging is performed due to any other reasons.
With regards to symptomatic CA, there may be non-specific symptoms indicating an intracranial lesion, possibly also prompting the suspicion of an increase of intracranial pressure. Patients may claim headaches and facial pain, present decreased levels of consciousness and/or an altered mental state. Ophthalmoplegia and visual impairment (consisting in blurred vision, diplopia and a restricted field of vision) are common and may be triggered by aneurysms located in the anterior or posterior communicating artery or the terminus of the internal carotid artery, among others. Cranial nerve palsies distinct from those of the optical, oculomotor, abducens and trochlear nerves as well as specific neurological deficits may also be observed. For instance, functional deficits of the lower cranial nerves may be seen in patients suffering from vertebrobasilar aneurysm. Cardiovascular or respiratory symptoms indicate compression of the brainstem, and in rare cases, endocrinologic disorders may dominate the clinical picture of CA.
Additionally, symptoms typically associated with hydrocephalus and meningitis may be observed. Nausea and vomiting and neck stiffness are signs of those diseases, and this also applies to some of the aforementioned pathological conditions.
With decreasing frequency, CA are detected in the anterior communicating artery, the terminus of the internal carotid artery, the posterior communicating artery and the anterior choroidal artery , and neuroimaging allows for their visualization, for the assessment of size, morphology and precise location. Angiography, carried out by means of 3D digital subtraction, computed tomography or magnetic resonance imaging, is generally indicated. The sensitivity of all techniques exceeds 95%. For a long time, 3D digital subtraction angiography has been the gold standard in CA diagnostics, but this approach is increasingly replaced by digital subtraction computed tomography angiography. Acquisition times and limited accessibility of the patient argue against magnetic resonance imaging. In any case, cerebral hemorrhages may not permit angiography to be realized within a reasonable time frame . Of note, it is not uncommon to detect multiple CA.
In order to assess the general condition of the patient, laboratory analyses of blood samples and measurement of coagulation times should be realized.
CA may be treated either conservatively or surgically, and a variety of factors should be considered before deciding for either of both options . In detail, the following aspects should be taken into account:
There is a risk inherent to surgery, although it may vary depending on the site of the aneurysm. In case of small, non-growing CA, the overall risk of rupture is low, and may indeed be lower than the aforementioned risk associated with a surgical intervention to repair the vasculopathy.
Conservative treatment basically consists in observation and regular follow-ups. With regards to drug therapy, corticosteroids, diuretics like mannitol and fibrinolytics have been applied in case of CA. Evidence supporting their efficacy is scarce and thus, their application is matter of ongoing debate. Thromboembolism due to CA may have detrimental consequences, though, and thus, at least the use of fibrinolytics is often recommended. Furthermore, control of hypertension by application of calcium channel blockers or alternative anti-hypertensive drugs should be pursued, and patients prone to seizures benefit from anticonvulsants.
Endovascular repair of CA presumably bears lower risks of recurrence than surgical clipping. Endovascular CA treatment comprises coiling of the respective bulge, while a clip encloses the neck of an aneurysm and thus isolates it from circulation. Relapses may be associated with incomplete clipping of aneurysms . Of note, blood pressure should be maintained in the upper physiological ranges after such interventions, since the risk of vasospasms and subsequent ischemia is rather high. Generally, vasospasms develop within three weeks after surgery.
CA are potentially life-threatening and death may occur due to cerebral hemorrhage and/or compression of brain structures. CA rupture is associated with particularly high mortality rates and large aneurysms are most likely to rupture. However, the prevalence of small CA by far exceeds that of large CA and thus, the majority of cerebral hemorrhages is indeed caused by small aneurysms. Besides size, aneurysm growth, a medical history of cerebral hemorrhages and vertebrobasilar aneurysms have been identified as prognostic factors of CA rupture . In sum, about one in four patients presenting with ruptured CA dies within 24 hours, a further 50% within one month .
CA may be congenital or acquired, whereby the latter are much more common than the former. In fact, a review of the available literature only reveals a few isolated case reports of congenital CA . Furthermore, a patient may be genetically predisposed for aneurysms and thus have a higher risk of developing this condition throughout life. The fact that familial accumulation of CA has been registered supports this statement. Hereditary connective tissue disorders like Marfan syndrome, for instance, may be associated with an increased elasticity of arteries and remodeling processes that progressively weaken the arterial wall. Nevertheless, most CA develop due to an unfavorable combination of acquired pathologies like atherosclerosis or vasculitis, and hypertension. Here, release of pro-inflammatory mediators and endogenous or bacterial proteinases provokes structural alterations of the vessel's wall, causes loss of flexibility and resistance . Bacteremia - in itself a complication of primary diseases like endocarditis - may be the trigger for these events. Depending on the severity of vascular lesions, single entities may or may not lead to CA formation. Increased blood pressure augments the mechanical stress on affected arteries and veins, and thus, favors further dilation of the aneurysm and possible rupture. Further pathologies that may lead to CA are metastasizing neoplasms , head trauma and sickle cell disease. Smoking as well as abuse of alcohol and illicit drugs have been shown to be enhancing etiologic factors.
It has been estimated that 2 to 5% of the overall population are affected by CA , whereby rising tendencies are primarily ascribed to improved diagnostics. Fortunately, the incidence of CA rupture is much lower. According to a recent retrospective study, 1 to 2% of CA rupture per year . Interestingly, prevalence of CA and incidence of cerebral hemorrhage due to CA vary with geographical location. Finnish people seem to be particularly susceptible to fatal rupture of CA . Often, women are reported to be more frequently affected by CA and rupture, but according to the cited study, this does not apply to all populations. The overall incidence of CA increases with age, and pediatric patients usually suffer from congenital disorders predisposing for aneurysm development .
Similar to aneurysms in other parts of the body, CA are focal, pathological dilations of blood vessels. In most cases, they have a regular, round to oval shape, and such aneurysms are generally referred to as saccular or berry aneurysms. They may be connected to the respective vessel through a narrow or wide neck, and this distinction is of importance with regards to the choice of therapy. Wide-necked aneurysms are absolute contraindications of endovascular coiling since the coil may prolapse into the vessel, which would cause an obstruction of blood flow.
The greatest risk associated with CA is that of rupture. Such an event generally leads to subarachnoid hemorrhage, but blood may also accumulate in subdural, intraventricular or intraparenchymal spaces. Both the initial lesion of the vessel's wall as well as the eventual rupture have been classified as inflammatory events . Due to an often unknown cause, pro-inflammatory cytokines and matrix metalloproteinases are released. They stimulate smooth muscle cell apoptosis and degradation of the extracellular matrix of the vessel's wall, which results in a focal weak spot. Because of ongoing pressure, this spot may dilate. Thus, the aneurysm grows, and the presence of a CA causes turbulences, favors thrombus formation and further degradation of the vessel's wall. Over the course of this iterative process, the CA may grow, and the pressure on adjacent tissue and the probability of rupture increases.
No specific measures can be recommended to prevent CA. Since early mortality is high and symptoms associated with CA may be rather non-specific, complete workups are of utmost importance to improve the patient's prognosis. In case an aneurysm is detected and treated, regular follow-ups are recommended to recognize aneurysm growth, CA rupture and possible recurrences.
In general, the term aneurysm describes a pathological dilation of a blood vessel. An aneurysm results from anomalies in the vessel's wall that renders it less resistant to the pressure it is constantly exposed to. Because the arterial blood pressure is higher than the venous blood pressure, aneurysms most commonly affect arteries. Virtually any blood vessel in the human body may dilate, and depending on its precise location, the corresponding bulge may compress adjacent structures. In case of cerebral aneurysm (CA), i.e., dilation of an intracranial blood vessel, pressure-induced lesions of adjacent tissues may have detrimental, life-threatening effects. Moreover, an aneurysm may rupture and the ensuing hemorrhage may add to the local mass effect or provoke hemodynamical failure. The former is of great importance in CA, the latter rather applies to aortic aneurysm and lesions of other major vessels.
Estimated prevalence rates of up to 5% of the general population may be surprising, but there is an explanation for the apparent contradiction between a high prevalence of CA and a low incidence of severe complications due to cerebral hemorrhage: The majority of CA measure less than a few millimeters in diameter and affected individuals remain asymptomatic. The risk of rupture and potentially fatal hemorrhages positively correlates with aneurysm size, but there is no cut-off value that would exclude the possibility of CA rupture.
According to the aforementioned epidemiological data, a specific treatment may or may not be indicated. Drug therapy has proven to be little helpful, and both endovascular coiling and surgical clipping are associated with considerable risks. Guidelines have been developed to aid the treating physician in their choice for either therapeutic approach.
The term intracranial aneurysm is often used synonymously to CA.
An aneurysm is a focal, pathological dilation of a blood vessel. Virtually all vessels may be affected, and if an aneurysm is encountered intracranially, it is referred to as cerebral aneurysm (CA).
Most CA develop due to an unfavorable combination of acquired pathologies like atherosclerosis, inflammation of blood vessels and hypertension. During an inflammatory reaction, mediators and enzymes are released that degrade the vessel's wall. It thus loses flexibility and resistance and eventually succumbs to blood pressure.
In some cases, CA may be congenital.
CA may not cause any symptoms at all, or they may merely lead to unspecific complaints like headaches, facial pain and visual impairment. Decreased levels of consciousness or an altered mental state may be observed. In some cases, neurological deficits may be registered.
Angiography, i.e., visualization of blood vessels, is the diagnostic approach of choice. There are distinct techniques that may be applied to depict intracranial vessels, and in fact, some CA may be detected on images obtained for unrelated reasons.
Patients incidentially diagnosed with small, non-growing CA may not need any specific therapy. Their condition should be monitored, though, and it is important they comply with regular follow-ups.
With regards to those patients presenting CA-associated symptoms, large, growing aneurysms or vasculopathies at risk of rupture, there are essentially two therapeutic options: Endovascular coiling or surgical clipping. Coils may be placed inside an aneurysm without the need for open surgery, but this technique may not be feasible in case of wide-necked CA. On the other hand, a clip may be placed on the neck of the aneurysm and isolate it from circulation.