Neurobehavioral Assessments of Cerebral Vasospasm - Animal Models of Acute Neurological Injuries: Injury and Mechanistic Assessments - page 542

assessing the patients' physical well-being (Hunt and Hess, WFNS,
Fisher, GOS; Tables 1 - 4 ) but not on their postoperative health,
which the World Health Organization defi ned as “a state of com-
plete physical, mental and social well-being and not merely the
absence of disease or infi rmity.”
The mortality and morbidity related to treating intracranial
aneurysms have declined signifi cantly, establishing clipping and
coiling as the standards of treatment ( 6 ). But a method of outcome
assessment, e.g., the GOS, has remained the same for decades,
despite a growing body of evidence that assessing patients' mobil-
ity, speech, cranial nerves, short- and long-term memory, and/or
sensory defi cits ( 7 ) is inadequate for properly assessing the disease
and its treatment impact on the patients' fate ( 8, 9 ). Furthermore,
the widely publicized advances of functional MRI and PET research
focused on behavioral changes have brought an end to the myth of
the “silent areas in the brain.” During the last 10 years, numerous
studies have revealed that the brain regions regarded as “clinically
silent” are not really silent. Nondominant hemisphere structures of
the frontal, temporal lobes, and temporo-parietal junction and
subcortical structures, such as the amygdala, striatum, etc., have
been shown to regulate our social, moral, religious, and even polit-
ical behaviors ( 10-12 ). These and other earlier observation of
behavioral changes ( 13 ) after aneurysm treatment raised the ques-
tion whether the GOS and the Quality Of Life (QOL) scale are
proper tools to assess the outcome after this treatment. It becomes
obvious that it is time to reevaluate these outcome measures and to
develop more adequate tools allowing proper assessment conse-
quences of both the surgical and endovascular treatments and
vasospasm. This should facilitate a more accurate outcome predic-
tion and allow for early intervention to prevent a poor outcome
such as that of Ms. CD.

3. Sources of
Neurobehavioral
Changes After
Aneurismal SAH

The second issue is that pathomechanisms that were responsible
for such a dramatic difference in the outcome of these two rela-
tively uncomplicated, successfully treated aneurysms remained
undefi ned. For many years following the publication of the seminal
paper by Weir ( 14 ), delayed cerebral vasospasm was recognized as
“a single, more important cause of clinical deterioration and poor
outcome after aneurismal SAH (aSAH) and successful treatment of
intracranial aneurysm” ( 6, 15, 16 ). However, recently, there has
been increased interest in other possible mechanisms that may con-
tribute to the unsatisfactory results of the intracranial aneurysm
treatment ( 17, 18 ). But, the question of what is the impact of initial