Biology Reference
In-Depth Information
Chapter 33
Introduction to Problems of Postsubarachnoid
Hemorrhage Delayed Cerebral Vasospasm
Ryszard M. Pluta
Abstract
The below citation that sounds like presented just yesterday, illustrates the problems clinicians and researchers
have been facing for more than a half-century. Over those years, we have learnt a lot about subarachnoid
hemorrhage, physiology, and pathophysiology of cerebral vessels, neurovascular unit, and neurophysiological
changes to the brain circuitry developing after aneurysmal subarachnoid hemorrhage (aSAH). Despite all
these fantastic and fascinating achievements, our understanding of vasospasm nature cannot be translated
into its successful treatment. In the following paragraphs, the problems related to vasospasm and its treatment
or prevention are presented.
Key words:
aSAH, Vasospasm, Delayed ischemic defi cits, NO, ET-1, Clazosentan
… if we could learn how to keep a patient safe from developing delayed cerebral
ischemic dysfunction, then the problem of surgery of ruptured aneurysms would
be nearly solved (
1
).
Aneurysmal subarachnoid hemorrhage (aSAH) accounts for
approximately 5% of all new strokes, affecting 2-10 out of 100,000
people each year with a slight preponderance in woman (1.6:1);
the mean age of affected people is 55 (
2
). aSAH is associated with
the high rates of initial (50%) and late mortality (up to 70%) and
signifi cant morbidity as more than 50% of survivors have cognitive
and/or functional impairments (
3
).
It has been known for more than a half-century that blood
produces spasm of the arteries (
4
) and that the blood clot presence
in the subarachnoid space after intracranial aneurysm rupture
(
5, 6
) leads to delayed cerebral vasospasm (
7
). But, it was Bryce
Weir who in his seminal paper (
8
) established the dominant
position of vasospasm as a cause of delayed ischemic neurological
defi cits responsible for a poor outcome in this disease.
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