Biology Reference
In-Depth Information
Chapter 35
Vasospasm: Measurement of Diameter, Perimeter,
and Wall Thickness
Mohammed Sabri and R. Loch Macdonald
Abstract
Cerebral vasospasm is a complication of subarachnoid hemorrhage (SAH) which can cause cerebral infarction
and poor outcome after SAH. Experimental investigations and experimental and clinical therapeutic maneu-
vers have endeavored to understand the pathogenesis of vasospasm and to develop treatments for it. The most
verifi able defi nition and characteristic of vasospasm is narrowing of the larger muscular intradural arteries of
the circle of Willis and hence, assessment of their lumen size is a key endpoint to be measured (this chapter).
Key words:
Morphometry, Subarachnoid hemorrhage, Vasospasm
1. Introduction
Cerebral vasospasm affects up to 70% of patients affl icted with
aneurysmal subarachnoid hemorrhage (SAH) and has its onset
about 3 days after SAH, is worst approximately 1 week SAH, and
resolves after about 14 days. It is an important cause of neurological
deterioration, disability and mortality and morbidity after (
1
).
Vasospasm is defi ned here as a reduction in diameter of an
intradural cerebral artery as seen on some type of angiogram (cath-
eter, computed or magnetic resonance imaging) or by cross-sectional
analysis. Vasospasm is for the most part a prolonged vascular
constriction that has been attributed to a number of insults that
range from the impairment and imbalance between constricting
and relaxing factors (reduced vasodilators and an increase in vaso-
constrictors), endothelial apoptosis, and microthrombotic-induced
disruption of the endothelium (
1-3
). The pathogenesis is not
completely worked out but clinical trials suggest smooth muscle
contraction mediated by endothelin acting on endothelin A receptors,
as well as calcium infl ux through voltage-gated calcium channels,
are key pathways (
4, 5
).
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