Branch vessel technology has made it technically feasible to preserve critical end-organ perfusion in the setting of CIA, SRA, and TAA aneurysms. The relatively low acute mortality rate and lack of short-term branch vessel loss are encouraging and merit further investigation. These advances have the potential to markedly diminish the complications associated with conventional management of complex aneurysms.

The placement of endovascular prostheses that maintain antegrade perfusion of one or both internal iliac arteries is feasible, and early results provide evidence for optimism with regard to safety and efficacy.

Component movement is commonly observed in modular devices, but clinical consequences are rare. The degree of overlap, aneurysm diameter, aneurysm length, and stentgraft diameter can be used to predict the risk of inter-component movement which may result in component separation.

1 The effect of chlormethiazole has been studied in a transient middle cerebral artery (MCA) occlusion model of cerebral ischaemia in the rat. The MCA was occluded for 1 h by use of an intraluminal suture technique, with reperfusion for 24 h following removal of the occluding filament. Neuronal damage was determined by measurement of the area of necrosis following Cresyl Violet staining of sections taken through the ischaemic region. 2 In the initial experiment, occlusion of the MCA produced a large volume of ischaemic damage in both cortex and striatum, characterized by necrosis and pyknosis (total volume of damage, 287 + 13 mm3; n = 9). Rats injected with chlormethiazole (1000 Jmol kg-', i.p.) 60 min before occlusion had a reduced volume of damage in both regions (104 ± 11 mm3; n = 9; P <0.001). 3 In a subsequent study systemic physiological parameters (heart rate, blood pressure, blood pH, blood gases and rectal temperature) were measured throughout the ischaemic period. 4 Chlormethiazole (1 000 mol kg-') pretreatment produced little change in systemic physiology and the neuroprotective effect of the drug when given 60 min prior to the MCA occlusion was confirmed. Chlormethiazole was also neuroprotective when given 10 min following the start of reperfusion (control group: 244 ± 52mm3, n = 10; chlormethiazole pretreatment group: 102 ± 23 mm3, n = 10; P<0.001; chlormethiazole post-ischaemia group: 122 ± 16 mm3; P < 0.001, n = 10). 5 It is concluded that chlormethiazole is an effective neuroprotective agent in this model of transient focal ischaemia. The observation that chlormethiazole is protective when given after reperfusion indicates that the effect of the drug is unlikely to be due to an alteration of intra-ischaemic cerebral blood flow, but is more probably a direct effect on the development of ischaemic damage.

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