An aneurysm is a focal dilatation of an arterial blood vessel. Luminal forces, such as high blood flow, shear stress and turbulence, are implicated in the pathogenesis of intracranial aneurysms, and luminal characteristics, such as sac size and morphology, are usually essential to the clinical decision-making process. Despite frequent clinical emphasis on the vessel lumen, however, the pathology underlying the formation, growth and rupture of an aneurysm mainly resides in the vessel wall. Research on the morphology and histopathology of the vessel wall reveals that intracranial aneurysms do not constitute a single disease, but are a shared manifestation of a wide range of diseases, each of which has a unique natural history and optimum therapy. This Review classifies intracranial aneurysms by vessel wall pathology, and demonstrates that understanding the morphology and pathology of this structure is important in determining the therapeutic approach. The article concludes that aneurysms represent a symptom of an underlying vascular disease rather than constituting a disease on their own.

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We assessed the diagnostic accuracy of multislice CT in detection of intracranial aneurysms in patients presenting with subarachnoid or intracranial haemorrhage. Multislice CT and multiplanar digital subtraction angiography (DSA) images were obtained in 50 consecutive patients presenting with subarachnoid (SAH) and/or intracranial haemorrhage and reviewed by three neuroradiologists for the number, size and site of any aneurysms. The CT data were assessed using multiplanar reformats (MPR), maximum-intensity projections (MIP), surface-shaded display (SSD) and volume-rendering (VRT). In conventional angiography 51 aneurysms were detected in 41 patients. CT angiography (CTA) showed up to 48 aneurysms in 39 patients, depending on the observer. The overall sensitivity of multislice CT was 83.3% for small (< 4 mm), 90.6% for medium-size (5-12 mm) and 100% for large (> 13 mm) aneurysms. The sensitivity of multislice CTA to medium-size and large intracranial aneurysm is within the upper part of the range reported for helical single-slice CT. However, as small aneurysms may not be found, DSA remains the standard technique for investigation of SAH.

The treatment of pial arteriovenous brain malformations is controversial. Little is yet known about their natural history, their pathomechanisms and the efficacy and risks of respective proposed treatments. It is known that only complete occlusion of the AVM can exclude future risk of haemorrhage and that the rates of curative embolisation of AVMs with an acceptable periprocedural risk are around 20 to 50%. As outlined in the present article, however, partial, targeted embolisation also plays a role. In acutely ruptured AVMs where the source of bleeding can be identified, targeted embolisation of this compartment may be able to secure the AVM prior to definitive treatment. In unruptured symptomatic AVMs targeted treatment may be employed if a defined pathomechanism can be identified that is related to the clinical symptoms and that can be cured with an acceptable risk via an endovascular approach depending on the individual AVM angioarchitecture. This review article gives examples of pathomechanisms and angioarchitectures that are amenable to this kind of treatment strategy.

The increase in local cerebral blood flow (LCBF) caused by hypercapnia may be mainly accomplished by raising the velocity of plasma and/or red blood cell (RBC) flow through the microvessels and not by perfusing more capillaries. This suggestion was tested in awake rats exposed to 8% CO2 and in control rats. LCBF was measured by the 14C-labeled iodoantipyrine method. The volume of blood in small parenchymal microvessels was estimated from the distribution spaces of 125I-labeled serum albumin (RISA) and 55Fe-labeled RBCs. Hypercapnia elevated LCBF 2.0- to 3.5-fold in the 40 brain areas studied, marginally raised the RBC spaces, and significantly increased the RISA and whole blood distribution spaces (approximately 25 and 19%, respectively). These changes in microvessel distribution volumes could be the result of perfusing a slightly larger fraction of capillaries (recruitment), increasing microvessel diameter somewhat, or both. With hypercapnia, the mean transit times fell to approximately 45% of control, which indicated that LCBF was mainly increased by raising the velocity of RBC and plasma flow through already perfused microvessels. Overall, few, if any, capillaries or other microvessels were recruited by hypercapnia.