Cerebral Vasospasm

There are essentially two principal end points in cerebrosvascular regulation: maintenance of an adequate supply of blood and energy-yielding substra tes to the brain, despite the imposition of physiological or pathological stresses such as hypoxemia or reduced perfusion pressure, and precise and rapid coupling of regional cerebral bload flow (CBF) to changes in neuronal r equ i r emen t s 3 2 . These two features of the cerebral circulation are met under a complex control of the cerebral vasculature by a still unknown mechanism of autoregulation Th is autoregulat ion depends on direct action of metabolites a n d / o r pressure stimuli in the smooth muscle vessel w a l l 2 6 , 2 8 , 3 2 . In several pathological conditions the cerebrovascular autoregulat ion can be impaired, not in toto, but in variable d e g r e e s 3 2 . Cerebral vessels no longer obey the physiological stimuli, but assume a s teady state tonus not coupled with the brain metabolism of their a rea of s u p p l y 3 9 . They can remain dilated or contracted. In the last case, the phe­ nomenon is known as cerebral vasospasm. Vasospasm can be due either to an abnormal responsiveness of the vascular smooth muscle cells or to abnormally high levels of endogenous vasoconstrictor s u b s t a n c e s 5 1 . It remains unclear as to whether vasospasm is a normal or abnormal contraction or failure relaxation of arterial smooth muscle cells or whether it represents a cytoarchitectural thickening in the vessel w a l l 2 3 . Cerebral vasospasm occurs in pathological cir­ cumstances such as migraine, subarachnoid hemorrhage (SAH) , head trauma, post-cerebral ischemia a n d / o r h y p o x i a 1 3 , 2 3 , 2 4 , 5 1 . Cerebral vasospasm is parti­ cularly important in SAH. While the surgical morbidity and mortality of uncom­ plicated cerebral aneurysm approaches that of a cho lecys tec tomy 2 4 , it has been demonstrated tha t the leading cause of death and disability in patients with aneurysmal SAH is cerebral v a s o s p a s m 2 3 . The cerebral vasospasm that follows SAH is a biphasis phenomenon. It consist of a relatively short early phase (minu tes ) 2 , reversible by antagonists of smooth muscle contraction and a late and long-lasting phase of spasm (weeks) , refractory to every muscle r e l a x a n t 2 3 , 4 5 . Each phase has a different p h y s i o p a t h o l o g y 2 3 , with similarities to other causes of cerebral vasospasm. Thus , SAH is a good model for the study of cerebral vasospasm. Much as been learned about the cerebral vasospasm tha t follows SAH since it w a s first described 30 years a g o 1 3 . This accumulated knowlege can ben applied to other diseases where cerebral vasospasm is present. It can also provide further understanding of the physiological control of cerebrovascular smooth m u s c l e 2 3 , 3 2 , 5 1 .