Although certain intrinsic and extrinsic factors have consistently been found to be associated with a higher risk of rupture in various studies, there is still a lack of a complete understanding of the natural history of intracranial aneurysms. In addition, in further analysis of the known risk factors, some discrepancies start to emerge. For example, although aneurysm size is a well-documented risk factor, the optimal cutoff size is yet to be defined. Aneurysm location can also affect rupture risk independently of size. In addition, with the increasing number of population-based studies, certain reports of interracial differences have emerged, further adding to the complexity of the matter 1) 2).
The study of intracranial aneurysms has grown at an astounding rate since Sir Charles Symond's association of hemorrhage within the subarachnoid space to intracranial aneurysms in 1923.
The first surgical treatment of an intracranial aneurysm with wrapping was made by Norman Dott in 1931 4) , but the first modern-era clipping procedure was performed by Walter Edward Dandy in 1937 5). Since then, the progressive evolution of devices, particularly the operating microscope, has resulted in intracranial surgery to secure aneurysms presenting with subarachnoid hemorrhage, or otherwise, becoming routine procedure.
The latest era of aneurysm treatment has seen the meteoric rise and acceptance of neuroendovascular treatment by interventional radiologists. Endosaccular obliteration by insertion of silver wire was first reported in 1941 6). During the 1970s and 1980s, the evolution of catheters and detachable devices, most importantly metal coils, resulted in the ability to secure intracranial aneurysms without the need for operative trauma or dissection to the brain. However, even the earliest studies of modern coiling techniques pointed towards some limitations of these techniques and suggested that some aneurysms might be more challenging or unsuitable for endovascular therapy 7) These difficulties were partially addressed over the 1990s by development of balloon and stent-assisted coiling techniques.
One of the most impressive studies on the outcomes of the two treatments for intracranial aneurysms, the International Subarachnoid Aneurysm Trial (ISAT) was presented in 2002 8). It suggested that the ruptured aneurysm treated endovascularly had a better one-year outcome, maintained at seven years, in terms of neurodisability and seizures. An increased risk of delayed rebleeding compared with the aneurysm treated surgically was seen. The practice of radiological follow up to identify the possible recurrence was encouraged, and rates of prophylactic retreatment following endovascular therapy were noted to be higher that for open surgery.
In parallel with these developments, advances in both the resolution and availability of neuroimaging modalities have led to an increased number of patients presenting with aneurysms that are considered asymptomatic. Epidemiological data have become accepted that offer year-on-year risk stratification of the risks of subarachnoid hemorrhage from such aneurysms 9). The modern neurosurgeon or neurologist is hence routinely asked to consider treatments for the unruptured, asymptomatic aneurysm, in addition to the emergency workload of those presenting with subarachnoid hemorrhage. The patient group over time has become younger, healthier, and better informed prior to presentation. Particularly those patients that present with an unruptured aneurysm after screening following the subarachnoid hemorrhage of a close relative may have strong psychological factors influencing their decisions to have treatment or not. They may be very keen to avoid the need for long-term follow up and eliminate worry. For these patients the issues of retreatment are very serious. For the experienced vascular neurosurgeon the operative conditions in the context of unruptured aneurysms are ideal and operative morbidities should be minimal. These factors, coupled with the recognition of the key differences not only in presentation but also in treatment goal, often combine to make surgical treatment of the unruptured aneurysm a preferable option 10).
Previous data from previous studies such as ISAT is difficult to apply to newer cohorts of patients. We now see a different patient group requiring aneurysm surgery. They have progressed from those presenting acutely in various states of disability, to a group that includes fewer such patients, but a greater proportion of recurrent or residual aneurysms post-coiling, and the unruptured group requiring treatment with the highest definitive success rate. Only further longitudinal studies of these newer groups of patients will guide us in time as to the precise outcomes 11).
Intracranial aneurysms are acquired lesions (5-10% of the population), a fraction of which rupture leading to subarachnoid hemorrhage with devastating consequences.
In a Korean population study, the standardized incidence of intracranial aneurysm was 52.2/100,000 person-years. Older age, female sex, hypertension, history of heart disease, and family history of stroke were independent risk factors for intracranial aneurysm 12).
Intracranial aneurysms (IAs) are rare in the general pediatric population and account for <2% of all cerebral aneurysms. Only 7 children with sickle hemoglobinopathy and IAs have been reported, the majority of which were discovered after rupture.
Very small intracranial aneurysm (< 3 mm)
Small intracranial aneurysm (< 5 and ≥ 3 mm)
Large intracranial aneurysm (12-25 mm)
Giant intracranial aneurysm (> 25 mm)
Until now, the exact etiology of intracranial aneurysms formation remains unclear. The most important factors predicting rupture are aneurysm size and site.
In addition to ambiental factors (smoking, excessive alcohol consumption and hypertension), epidemiological studies have demonstrated a familiar influence contributing to the pathogenesis of intracranial aneurysms, with increased frequency in first- and second-degree relatives of people with subarachnoid hemorrhage.
Data suggest that macrophage-derived Matrix metalloproteinase 2 and Matrix metalloproteinase 9, may play an important role in the progression of intracranial aneurysms. The findings will shed a new light into the pathogenesis of cerebral aneurysms and highlight the importance of inflammatory response causing the degeneration of extracellular matrix in the process of this disease 13).
Investigations strongly suggest that the pathophysiology is closely associated with chronic inflammation in vascular walls. Nuclear factor kappaB (NF-kappaB) has a key role in the formation and progression
Children with Sickle Cell Disease (SCD) are at risk for developing multiple intracranial aneurysms, and a high index of suspicion must be maintained during the interpretation of routine magnetic resonance imaging or angiography of the brain 14).
Dental bacterial DNA can be found using a quantitative polymerase chain reaction in both ruptured and unruptured aneurysm walls, suggesting that bacterial DNA plays a role in the pathogenesis of cerebral aneurysms in general, rather than only in ruptured aneurysms 15).
The clinical presentation is varied, ranging from asymptomatic lesions to those presenting with major rupture
The low incidence of subarachnoid hemorrhage in comparison with the prevalence of unruptured IAs suggests that the vast majority of intracranial aneurysms do not rupture and that identifying those at highest risk is important in defining the optimal management.
Intracerebral hematoma (ICH) with subarachnoid hemorrhage (SAH) indicates a unique feature of intracranial aneurysm rupture since the aneurysm is in the subarachnoid space and separated from the brain by pia mater.
Treatment of cerebral aneurysms (ed by Takakura K)