Neurobehavioral Assessments of Cerebral Vasospasm - Animal Models of Acute Neurological Injuries: Injury and Mechanistic Assessments - page 567

only means to study certain important areas of cortex, given that
some areas may not be shared with other mammals. For example,
it has been argued that parts of our highest-order prefrontal cortex
may have evolved in the primate lineage, and thus may not be
shared with other animals, such as rodents ( 260, 261 ). In such
cases, only a nonhuman primate model would be available to study
the impact of cerebral vasospasms on higher-order cognitive func-
tions in a systematic and comprehensive way.

8. Closing
Remarks and
Limitations

During the last several years, it has become obvious that there is a
signifi cant gap in assessing the outcome after treatment of aSAH.
For years, neurosurgeons and neurointerventionalists have been
focused on the neurological functionality of patients as a main
measure to assess their success in treating the intracranial aneu-
rysms. Most often, the GOS is used to assess the results of the
treatment. But, individual experience, sporadic series of patients
operated in a delayed fashion, as well as the patients operated upon
before aneurysm rupture pointed to the need of better neurologi-
cal, psychological, and QOL assessments. Thus, GOS become
inadequate in the face of everyday life requirements for many
patients. As a result, more precise and in-depth assessments of neu-
robehavioral changes have been advised and have slowly emerged
as necessary and more adequate tools ( 8 ). Unfortunately, we do
not have a clear understanding of the pathomechanisms of neu-
robehavioral changes after aSAH and we lack the proper experi-
mental tool to investigate them. It is obvious that to address this
issue we need to develop proper research tools by redirecting
scientifi c efforts away from studying vasospasm to more widely
addressing the extent of brain damage evoked by aSAH ( 17, 18, 20 ).
Other reasons justifying experimental neurobehavioral studies in
animal models of SAH are (1) objectifying the diffi cult-to-assess
subjective complains of patients; (2) recognizing pathophysio-
logical mechanisms leading to behavioral changes after SAH; and
(3) realizing the important components of psychobehavioral changes
evoked by aSAH versus vasospasm versus DIND. These are impor-
tant goals because in the patient population, there are many com-
pounding and confusing factors that obscure or even prevent
separating their infl uence on overall outcome and neurobehavior.
Among them are (1) locating the bleeding; (2) determining
the amount of subarachnoid blood; (3) noting the presence of
intraventricular blood; (4) surgical manipulation, transient clip-
ping, arteriography, and endovascular approach; (5) hydrocepha-
lus; and (6) other secondary complications of SAH and surgery.
Fortunately, the animal models that have been developed to study
delayed cerebral vasospasm, especially the small animal models that