Types of unruptured cerebral aneurysms reviewed from operation video-recordings

Abstract

To estimate the proportion of unruptured cerebral aneurysms with thin-walled sac, we have analyzed the operative findings of 78 incidental cerebral aneurysms found in 51 consecutive surgical cases by reviewing of intra-operative videotape recordings. Among 78 unruptured aneurysms, 23 (30%) were evaluated as thick-walled aneurysms (Type A), 39 (50%) with partially thin-walled sac (Type B) and 16 (20%) with entirely thin wall sacs (Type C). The mean size of Type A aneurysms was 10.4 mm (ranging from 3 to 22 mm), in Type B it was 9.8 mm (ranging 4 to 25 mm) and in Type C it was 4.4 mm (between 2-12 mm). Approximately two-thirds of Type C aneurysms were 4 mm in size or smaller, and Type C aneurysms were significantly smaller than Type A aneurysms. In summary, this preliminary study has provided two original data. 1) About 70% of incidental unruptured aneurysms have a partially or entirely thin-walled sac. 2) Many of the small aneurysms have an entirely thin sac. Assuming that thin-walled aneurysms are at a high risk of subsequent rupture, the surgical intervention for incidental unruptured aneurysms may be recommended irrespective of their size if the surgical risk is considered low.

High WSS or Low WSS? Complex Interactions of Hemodynamics with Intracranial Aneurysm Initiation, Growth, and Rupture: Toward a Unifying Hypothesis

“…This concept is illustrated in Fig 5. Small and transparent type I aneurysms develop relatively quickly. 68 Their walls lack inflammatory cells and other cell types, as demonstrated by intraoperative [47][48][49] and postmortem studies. [52][53][54] It is possible that they are formed by impinging flow through the high-WSS-driven degradation mechanisms, as illustrated on the left side of Fig 5. The resident mural cells produce matrix maetalloproteinases under high WSS conditions, leading to significant ECM degradation and cell death by anoikis (apoptosis due to loss of ECM anchorage).…”

“…19,54 On the other hand, the large, thick-walled, atherosclerotic type II aneurysms appear to have developed during a longer period of time through various attempts to heal the sac. [47][48][49] Indeed, most inflammatory cells found in aneurysm specimens came from this type of aneurysm. [52][53][54] We therefore conjecture that the natural history of type II aneurysms (after initiation) is dominated by the inflammatory-cell-mediated pathway, as illustrated on the right side of Fig 5. The destructive remodeling here is accompanied by increased inflammatory cell infiltration and smooth muscle cell proliferation, especially after atherosclerotic plaque and/or thrombus formation.…”

“…Three principal aneurysm pheno- types have been reported from intraoperative observation of unruptured intracranial aneurysms. [47][48][49] The first types are small aneurysms (Ͻ4 mm) with uniformly thin, smooth, hypocellular, translucent walls, through which reddish blood flow can be visualized at the time of surgical clipping. We refer to these as type I aneurysms (an example is seen in Fig 3A).…”

“…We refer to these as type II aneurysms (an example is seen in Fig 3D). The third types are medium-sized aneurysms with a combination of thin-and thickwalled characteristics in different regions 47,49 or with intermediate wall thickness. 50 We refer to these as a combination type (examples are seen in Fig 3B, -C).…”

Colocalization of thin-walled dome regions with low hemodynamic wall shear stress in unruptured cerebral aneurysms

“…1,13,20,24 The net effect of this complex remodeling process is a modification in wall thickness that is readily visible during microsurgical dissection and observation, with thinning regions of the aneurysm dome identified during surgical observation and correlated with the site of rupture. 2,14,15,18,25 These changes provide a rich source of readily quantifiable data that can be used to de-scribe systematic intraaneurysmal differences that vary in association with risk factors such as patient sex and aneurysm size. 18 As of yet, there have been no data on the relationship between local hemodynamic variables within the aneurysm dome and direct in vivo observation of aneurysm wall properties in human studies.…”