Neurobehavioral Assessments of Cerebral Vasospasm - Animal Models of Acute Neurological Injuries: Injury and Mechanistic Assessments - page 546

results and (4) a lack of difference in the extent of neurobehavioral
defi cits between patients operated for aSAH and those with aSAH
but without surgery ( 44 ). Furthermore, the International Study of
Unruptured Aneurysms revealed that patients do better when
operated upon before the aneurysm ruptures producing aSAH
( 49 ). These fi ndings demonstrate the infl uence of early versus late
aSAH-related events on outcome ( 17, 18, 20 ). Practical consequences
of all these fi ndings are diffi cult to overestimate. The patient whose
clinical status was assessed at GOS 5 after aSAH and aneurysm
treatment may still need signifi cant neuropsychological diagnostics
and rehabilitation. Thus, there is no doubt that establishing the
cause and pathophysiology of reported neurobehavioral changes
should facilitate the diagnostics and treatment options for aSAH.
A properly designed experimental model could provide in-depth
insight into causes, pathophysiology, and pathomechanisms of
these defi cits, thereby providing a tool to develop targeted treat-
ments and rehabilitation.

5. Experimental
Models to Study
Outcome
of Aneurismal SAH

For many years, we have developed excellent experimental models
of SAH, but all were focused on studying the development, pres-
ence, and effects of delayed cerebral vasospasm ( 50 ). The focus was
so narrow because these models were also supposed to address
“vasospastic syndrome,” also known as “delayed cerebral dysfunc-
tion” ( 51 ) or DIND, since it was evoked by the presence of cere-
bral vasospasm ( 14 ). Recently, this dogma has been questioned
and slowly abandoned ( 17, 18, 20 ). The new research approaches
have refocused on the neurobehavioral changes evoked by aSAH
acutely because of the severity of the initial SAH or the delayed
development due to the prolonged presence of blood clot(s) on
the surface of the brain. Both the acute and delayed mechanisms
are at least as important as vasospasm and its neurological conse-
quences in assessing the effects of treatment for intracranial aneu-
rysms. Nevertheless, none of the models addresses the infl uence of
these events on neurobehavior because all were developed to study
delayed cerebral vasospasm ( 52 ).

There are numerous animal models that mimic the clinical situation
of aSAH. A detailed description of these models can be found else-
where. We also recommend two recently published excellent
reviews on this topic ( 52, 53 ). Table 7 presents the summary of the

5.1. aSAH Animal
Models