Biology Reference
In-Depth Information
The neurological outcome following SAH is dependent on
several factors, including initial SAH severity, preoperative medical
management, intraoperative variables, and incidence of complica-
tions. But, it was delayed cerebral vasospasm and subsequent
delayed ischemic neurological defi cits that were recognized, and
widely accepted, as some of the most serious complications occur-
ring in patients who initially survive an aSAH ( 2, 8 ).
Arteriographic vasospasm occurs up to 70% ( 9 ) and clinical
vasospasm (delayed ischemic neurological defi cits) occurs in
25-30% of patients who survive the acute phase of aSAH. These
two seemingly inseparable events are responsible for lasting neuro-
logical impairment or death in as many as one-third of patients
after aSAH ( 2, 9 ). But, relatively low numbers of patients (<50%
( 9 )) with arteriographic vasospasm experience clinical deteriora-
tion or clinical vasospasm ( 10 ). This discrepancy was recognized
years ago when Bloor and colleagues wrote: “(s)ome patients with
severe spasm of the circle of Willis have very little alterations
of cerebral blood fl ow, whereas some patients with minimal spasm
of the circle of Willis have a marked reduction in cerebral blood
fl ow; the critical vessels causing a reduction in fl ow may be small
penetrating arteries and arterioles”( 11 ).
It becomes obvious that the issue of vasospasm and its role in
pathophysiology of delayed ischemic defi cits, or clinical vasospasm,
as well as its contribution to the poor outcome could be signifi -
cantly over-rated ( 12, 13 ). Since early seventies clinicians, like the
one cited above, reported the incidence of delayed ischemic neuro-
logical defi cits without the presence of vasospasm ( 11 ). These
reports were dismissed or treated as anomalies until the Clazosentan
study (a blocker of the endothelin-1 type A receptor) confi rmed,
for the fi rst time in clinical setting, that a successful prevention of
vasospasm did not translate to improvement of outcome ( 14 ). It is
beyond the scope of this short review to discuss the reason(s) for
this unexpected failure, but most importantly it led to increased
interest in other pathomechanisms of aSAH that may lead to
delayed cerebral ischemia. These include the long-time known
ICP-related “no fl ow” phenomenon that leads to the “no-refl ow,”
or infl ammatory changes ( 15, 16 ), or more recently, apoptosis/
necrosis of vessels and neurons ( 17-20 ), and recently rediscovered
neurotoxic effect of hemoglobin ( 21, 22 ), as well as also well-
known electrolyte imbalance and oxidative stress evoked by tran-
sient ischemia after aSAH ( 13, 20 ). Among these, a signifi cant
attention has been recently focused on the reversed-coupling of
brain activity and blood fl ow regulation introduced by Jens Dreier
and colleagues ( 23 ), that leads to cortical ischemia in a delayed
fashion, and which is discussed in detail elsewhere in this topic. All
of these recent fi ndings are shifting attention from vasospasm being
a main culprit responsible for poor outcome to the new “greener”
more promising fi elds.
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