PCT in Vasospasm After SAH 43 (papaverine hydrochloride, Eli Lilly and Co., Indianapolis, IN) i.e., areas of vasospasm which are still asymptomatic owing to was infused via a microcatheter in the left MCA to treat spasm intact autoregulation but may become symptomatic over time. of the proximal M2 segments. Within 2 days, her aphasia dis- Further research is warranted to determine if angioplasty of appeared. PCT was repeated and showed symmetric, normal- spastic vessels supplying these areas may improve outcome of ized CBV, CBF, and MTT values (Figure 1D–F). patients with SAH. PCT has several limitations, including restricted anatomic Case Discussion coverage and lack of full validation of its accuracy, reliability, This case illustrates the value of PCT in demonstrating the and reproducibility of quantitative results (7,16,19,20). With effect of transluminal balloon angioplasty on cerebral perfu- our multislice CT scanner, we were able to use a collimation of sion in a patient with vasospasm after SAH. Before angio- 4 × 5 mm and to obtain 2 × 10 mm reconstructed slices. By per- plasty, decreased to normal CBF and increased CBV and MTT forming PCT at two different levels we could obtain 4 cm brain were identified in the left MCA territory, indicating tissue at coverage. With 16-, 32- and 64-slice CT scanners, a larger brain risk for cerebral infarction with intact autoregulation. After an- coverage will be possible. Quantitation is strongly dependent gioplasty, perfusion parameters returned to normal values and on the choice of the venous ROI location (19,20). Different were symmetric. ROI locations within the same vein may result in significantly Cerebral vasospasm is a frequent complication in patients different CBV and CBF values (19). The venous ROI with the with aneurysmal SAH (1). In 50% of cases it is manifested by greatest peak enhancement value should be chosen, as is done delayed neurologic deficits related to ischemia, with progres- in the software used in this study to limit variability and in- sion to infarction in approximately one-half of the symptomatic crease quality of PCT images (19). With proper ROI selections cases (1,8). Angioplasty for vasospasm may significantly reduce a good correlation between quantitative PCT maps and morbidity and mortality if performed early after medical ther- xenon-CT and positron emission tomography (PET) studies apy has failed (1,10). It is, albeit rarely, also associated with se- was found, as described in previous reports (3,5). vere complications, such as vessel rupture, and should there- This case illustrates the value of PCT for monitoring treat- fore only be used in those patients in whom vasospasm causes ment effects in patients with symptomatic vasospasm. This cerebral ischemia (1,8). Because delayed neurologic deficits fol- minimally invasive technique is widely available and requires lowing SAH may have different causes, including hydrocepha- only a modest radiation dose. lus, hemorrhage, edema, metabolic factors, and ischemia (12), it is important to identify those patients with vasospasm who most likely will benefit from angioplasty. Although TCD may aid in the determination of vasospasm, it does not necessarily assist in the identification of ischemia (12). SPECT (2), Xe-CT (3), and PET (4,5) are reliable methods for the determination of cerebral perfusion, but these techniques are cumbersome and not widely available. PCT can be combined with unenhanced CT, which is routinely performed for follow-up of patients with SAH (7). Nabavi et al. used this technique for monitoring cerebral perfusion after aneurysmal SAH (6). They found signi- ficant differences in CBF and CBV between patients with signif- icant and absent or minor vasospasm and between patients with and without a presumed vasospasm-related infarct. They could not, however, define a PCT-threshold for cerebral infarct by using PCT, because of the use of relatively large ROIs, caus- ing volume averaging with normal and ischemic tissue (6,16). The findings of the current report are consistent with results described by Grubb et al. (17). The system of autoregulation is reflected by PCT findings in patients with cerebral ischemia (18). A mild reduction in cerebral perfusion pressure is associ- ated with a compensatory dilatation of cerebral blood vessels. Under these circumstances, measurements of CBF remain within normal range, while those of CBV and MTT increase. As perfusion pressure falls, normal CBF cannot be maintained, despite further vasodilatation (oligemia or misery perfusion). When perfusion pressure falls below a threshold of approxi- mately 20 mL per 100 g and per minute, cerebral metabolism is severely impaired (ischemia). The development of subsequent irreversible damage (infarction) is not only dependent on the absolute perfusion value but also on the time the tissue has been ischemic. Irreversible damage is associated with loss of autoregulatory vasodilatation and therefore reduced CBV (18). PCT may also be valuable in detecting subclinical ischemia, References 1. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med 2006;354:387–396. 2. Lewis DH, Eskridge JM, Newell DW, et al. Brain SPECT and effect of cerebral angioplasty in delayed ischemia due to vaso- spasm. J Nucl Med 1992:33:1789–1796. 3. Wintermark M, Maeder P, Thiran J-Ph, et al. Simultaneous measurements of regional cerebral blood flows by perfusion-CT and stable xenon-CT: a validation study. AJNR Am J Neuroradiol 2001;22:905–914. 4. Powers WJ, Grubb RL, Baker RP, Mintun MA, Raichle ME. Regional cerebral blood flow and reversible ischemia due to vasospasm. Determination by positron emission tomography. J Neurosurg 1985;62:539–546. 5. Kudo K, Terae S, Katoh C, et al. Quantitative cerebral blood flow measurement with dynamic perfusion CT using the vascular- pixel elimination method: comparison with H2(15)O positron emission tomography. AJNR Am J Neuroradiol 2003;24:419–426. 6. Nabavi DG, LeBlanc LM, Baxter B, et al. Monitoring cerebral perfusion after subarachnoid hemorrhage using CT. Neuro- radiology 2001;43:7–16. 7. Wintermark M, Ko NU, Smith WS, Liu S, Higashida RT, Dillon WP. Vasospasm after subarachnoid hemorrhage: utility of perfu- sion CT and CT angiography on diagnosis and management. AJNR Am J Neuroradiol 2006;27:26–34. 8. Sen J, Belli A, Albon H, Morgan L, Petzold A, Kitchen N. Triple-H therapy in the management of aneurysmal subarchnoid haemor- rhage. Lancet Neurology 2003;2:614–620. 9. Lee Kh, Lukovits T, Friedman JA. “Triple-H” therapy for cerebral vasospasm following subarachnoid hemorrhage. Neurocrit Care 2006;4:68–76. Diederik van de Beek received funding from the Meningitis Research Foundation UK, the Jan Meerwaldt Foundation, and the Netherlands Organization of Scientific Research (Rubicon); no conflicts of interest. Acknowledgments Neurocritical Care ♦ Volume 6, 2007