Cerebrovascular reserve

Guckel FJ, Brix G, Schmiedek P et al (1996) Cerebrovascular reserve capacity in patients with occlusive cerebrovascular disease assessment with dynamic susceptibility contrast-enhanced MR imaging and the acetazolamide stimulation test. Radiology 201 405-412... 

Naylor AR, Merrick MV, Sandercock PAG et al. (1993a). Serial imaging of the carotid bifurcation and cerebrovascular reserve after carotid endarterectomy. British Journal of Surgery 80 1278-1282... 

In patients with known chronic cerebral ischemia related to underlying carotid artery stenotic lesions, CBF is usually preserved, at least initially, because of the cerebrovascular reserve. The cerebrovascular reserve represents the vasodilatation ability of cerebral arteries to compensate for a CBF tending to decrease and maintain this CBF at a normal level. In patients with chronic cerebral vascular disorders, it is necessary to quantify the residual cerebrovascular reserve and to distinguish tissue that has used only a limited fraction of its vasodilatation ability and still has cerebrovascular reserve available as a bulfer from tissue that has exhausted its vasodilatation ability and cerebrovascular reserve. The latter is at risk of ischemia, which can be triggered by any hemodynamic stress, and requires intervention to increased CBF, usually through carotid stenosis surgery or endovascular treatment, or extracranial-intracranial artery bypass (Nariai et al. 1995). 

Hemodynamic stress can be mimicked by using a tolerance test such as acetazolamide administration in conjunction with quantitative measurement of CBF. Although the exact mechanism of action is uncertain, acetazolamide causes vasodilatation of normal cerebral arteries and an increase in CBF in the corresponding territory. Patients with impaired cerebrovascular reserve, however, are aheady maximally vasodilated due to the response of cerebral autoregulatory mechanisms, and thus cannot respond further to acetazolamide. CBF does not increase, but remains stable or even decreases, because of a steal phenomenon by the healthy arteries (Nariai et al. 1995). Acetazolamide is generally well tolerated, with the most common side effects being cir-cumoral numbness, paresthesias, and headache. One case of acetazolamide-associated reversible ischemia has been reported (Komiyama et al. 1997). 

The quantitative results potentially available with PCT may provide an advantage over qualitative techniques such as SPECT and perfusion MR imaging. The ability to measure CBV and MTT may also be an added advantage of PCT. Indeed, a recent study demonstrated that the degree of impairment in cerebrovascular reserve, as assessed by chnical history, correlated most closely with the change in MTT in response to acetazolamide (Smith et al. 2008). This study also showed that increased baseline MTT values may be a static, quantitative indicator of compromised cerebrovascular reserve in at-risk territories (Smith et al. 2008). 

Smith LM, Elkins JS, Dillon WP, Schaeffer S, Wintermark M (2008) Perfusion-CT assessment of the cerebrovascular reserve a revisit to the acetazolamide challenges. J Neuroradiol 21 1441-1449... 

---