Neuroimaging Assessment of Cerebral Vasospasm - Animal Models of Acute Neurological Injuries: Injury and Mechanistic Assessments - page 579

Chapter 46
Neuroimaging Assessment of Cerebral Vasospasm
Kaisorn L. Chaichana , Gustavo Pradilla , and Rafael J. Tamargo
Abstract
Cerebral vasospasm following aneurysmal SAH can lead to devastating neurological sequelae in humans.
The pathophysiology of this phenomenon has yet to be fully elucidated, primarily because of limitations of
current experimental models. Animal models, which rely on in vitro examination of the cerebral arteries,
have conventionally been the primary method for studying this condition. Imaging technologies are evolv-
ing which allow for in vivo evaluation of cerebral vasospasm in animals. These technologies include tran-
scranial Doppler (TCD), computer tomorgraphy (CT) with angiography or perfusion, magnetic resonance
imaging with angriography or spectroscopy, and positron emission tomography. This chapter reviews these
imaging modalities which provide promising new options for in vivo examination of vasospasm, in both
animal and human models.
Key words: Animal, Angiography, Cerebral vasospasm, Computed tomography angiography,
Magnetic resonance angiography, Transcranial Doppler
1. Introduction
Chronic vasospasm is the leading cause of morbidity and mortal-
ity following aneurysmal subarachnoid hemorrhage (aSAH) ( 1 ).
In humans, this phenomenon is biphasic ( 1 ). Typically, the acute
phase occurs 3-4 h after the hemorrhage and resolves rapidly; the
chronic phase occurs 3-14 days later ( 1 ). During the chronic
phase, cerebral arteries become persistently narrowed, which can
lead to ischemia, neurological defi cits, and death in 20-40% of
patients ( 1 ). This sustained arterial narrowing has also been
reported in meningitis, traumatic brain injuries, and post-operative
craniotomies ( 2 ).
The etiology of chronic vasospasm remains unclear. Current
hypotheses include endothelial dysfunction secondary to arterial
wall infl ammation and transendothelial migration of macrophages
and neutrophils, nitric oxide (NO) scavenging by blood degrada-
tion products, such as oxyhemoglobin, NO depletion secondary