Partial aortic obstruction improves cerebral
                  perfusion and clinical symptoms in patients
Partial aortic obstruction: P. Lylyk et al.

be treated with a novel device (CoAxia, Inc. NeuroFloTM
catheter) designed to...
Partial aortic obstruction: P. Lylyk et al.

Figure 2: (A) Aortogram in AP view showing points of measurement (arrows)....
Partial aortic obstruction: P. Lylyk et al.

Figure 3: Baseline parenchymogram showing a regional perfusion deficit (arr...
Partial aortic obstruction: P. Lylyk et al.

Figure 4: Parenchymogram after procedure showing improvement of focal perf...
Partial aortic obstruction: P. Lylyk et al.

vasospasm on the left A2 and M2, with a filling regional        address blood ...
Partial aortic obstruction: P. Lylyk et al.

failure, cerebral edema and even cerebral hemorrhage,                        ...
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Partial aortic obstruction improves cerebral perfusion and ...

  1. 1. Partial aortic obstruction improves cerebral perfusion and clinical symptoms in patients with symptomatic vasospasm Pedro Lylyk, Jose F. Vila, Carlos Miranda, Angel Ferrario, Ricardo Romero and ´ Jose E. Cohen ´ Department of Neurosurgery, Endovascular Neurosurgery and Interventional Neuroradiology, ENERI Clınica Medica Belgrano Buenos Aires, Argentina ´ ´ Objective: Stroke studies in animals showed that aortic obstruction increases cerebral blood flow (CBF) and reduces infarct size. In this study we evaluate the safety and efficacy of a device providing partial and transitory aortic obstruction. Methods: We report the results in 24 selected patients with symptomatic vasospasm by aneurysmal subarachnoid hemorrhage treated by partial and transitory aortic obstruction with a novel device (NeuroFloTM, CoAxia, MN). Aneurysms were secured by coils prior to the procedure. We studied the adverse effects related to the aorta-obstructing device, and changes in CBF and neurological outcome. Results: Mean flow velocity increased in both middle cerebral arteries over 15%, and the score in the National Institute of Health Stroke Scale decreased >2 point in 20 patients (83%). During the procedure, three patients developed symptoms that were controlled. At 30 days follow-up, three patients had 6 points (unrelated death), three had 3 points, six had 1 point, and 12 had 0 points, in the modified Rankin scale. Discussion: Partial aortic obstruction was safe, the cerebral blood flow increased without inducing significant hypertension and the neurological defects improved in most of the patients. Efficacy with a better level of evidence will be determined by a randomized study. [Neurol Res 2005; 27: S129–S135] Keywords: Controlled aortic obstruction; subarachnoid hemorrhage; symptomatic vasospasm; vasospasm; vasospasm treatment. INTRODUCTION to medical therapy. Angioplasty can increase a vessel’s Vasospasm is the leading cause of death and disability caliber, and has been shown to improve focal cerebral in patients surviving aneurysmal subarachnoid hemor- perfusion and clinical symptoms without inducing hyper- rhage (SAH). Angiographic vasospasm occurs in as tension4–7. Since the endovascular treatment requires an many as two-thirds of patients beginning about 3 days interventional radiologist, its application is restricted to following bleeding1 and about one-half of afflicted specialized centers. The role of angioplasty appears to be patients will develop focal neurological symptoms. limited to focal and proximal vasospasm of the larger Untreated, 25% of patients with symptomatic vasos- arteries at the base of the brain8, which leaves untreated the pasm die2,3, and a further 40% are permanently substantial number of patients whose symptoms are due to disabled by single or multiple cerebral infarcts2. narrowing of the resistance arterioles of the microcircula- Currently, the most widely used treatment for symp- tion (distal vasospasm)4. On perfusion scanning, these tomatic vasospasm is hypervolemia and hemodilution patients have evidence of diffuse cortical dysfunction and combined with pharmacologically induced hyperten- patchy, diffuse perfusion abnormalities9,10. Below critical sion (Triple-H therapy), despite the fact that evidence threshold values, such perfusion defects evolve into of efficacy for this regimen is lacking in controlled infarcts, many of which are clinically silent. studies4. Triple-H therapy can be difficult to regulate for In this study, we analysed the use of a novel intra- any length of time and poor tolerance, and the frequent aortic balloon to create partial aortic obstruction, which cardiac and cerebral complications limit its use. results in an increase of global cerebral blood flow Cerebral angioplasty, with or without intra-arterial (CBF) without significantly raising blood pressure, for vasodilators, has recently emerged as an alternative treating patients with symptomatic vasospasm. method for the treatment of patients who failed to respond Correspondence and reprint requests to: Dr Pedro Lylyk, ENERI Av. SUBJECTS AND METHODS Del Libertador 6647, C1428ARJ, Buenos Aires, Argentina [plylyk@lylyk. We prospectively enrolled 24 consecutive patients with]. symptomatic vasospasm following aneurismal SAH, to # 2005 W. S. Maney & Son Ltd Neurological Research, 2005, Volume 27, Supplement 1 S129 10.1179/016164105X35512
  2. 2. Partial aortic obstruction: P. Lylyk et al. be treated with a novel device (CoAxia, Inc. NeuroFloTM catheter) designed to augment CBF without raising blood pressure. The primary endpoint was assessment of the safety of the catheter based on the incidence rate of device-related adverse events during a 30-day follow- up. The secondary endpoints were: N device technical success; N augmentation of CBF expressed by 15% or more Figure 1: Dual balloon device for partial aortic obstruction increase in mean flow velocity (Mfv) in both middle (NeuroFloTM, Coaxia, MN) cerebral arteries (MCA) via trans-cranial Doppler (TCD) during procedure; N INR.1.7 or PTT.1.5 local control, or platelet count N improved CBF, expressed as a reduction of regional ,100.000; area with circulatory defects in the cerebral parench- ymography (CP), or increase in the diameter of the N aortic diameter suprarenal .27 mm, infrarenal .23 mm or less than 11 mm (within 6 cm above or arterial segment with vasospasm in the digital below the midpoint of the renal arteries); subtraction angiography (DSA), post-procedure; N history of aortic aneurysm on baseline fluoroscopy or N neurological improvement, expressed by post proce- ultrasound (aortic aneurysm defined as local dilation dure reduction of 2 or more points in the National 1.56 diameter of aorta, or aortic diameter .35 mm); Institute of Health Stroke Scale (NIHSS) score; N co-morbid condition likely to complicate therapy, N neurological outcome, as described by modified e.g. history of renal failure, or creatinine .2, pelvic Rankin (mR) score at 30 days; abdominal mass likely to compress distal aorta, N mortality-related and unrelated to use of the device. dementia severe enough to prevent valid consent, end stage AIDS, history of claudicating; Selection criteria N cardiac disease, e.g. myocardial infarction within 6 months, congestive heart failure (old or current), rest Eligible patients were defined as those who meet all angina, angina, or anti angina medications, evidence of the inclusion criteria and none of the exclusion of aortic regurgitation, recent or current supraventri- criteria. Inclusion criteria: cular or ventricular tachycardia on ECG, ejection fraction ,30%, severe aortic regurgitation (>3z), N age >18 years old; systolic BP.200 or ,100 mmHg on three measures N focal neurological deficit >2 point as measured by taken 3 minutes apart, hypertension requiring nitro- NIHSS; prusside or similar aggressive agent, or continuous IV N SAH due to aneurysm rupture; therapy to maintain systolic BP below 200 mmHg; N secured aneurysm (endovascular or clipped) prior to N carotid stenosis .50%; the procedure; N symptomatic vasospasm confirmed by TCD (defined N medical conditions likely to interfere with catheter as a mean cerebral blood flow velocity (CBFvm) placement or patient assessment. greater than 120 cm/second), or DSA (focally nar- An Institutional Review Board and an independent rowed normal diameter, or delay in capillary bed Ethical Committee approved the protocol. Patients opacification visualized on AP parenchymography); provided informed consent. The study was sponsored N informed consent. by CoAxia, Inc. Maple Grove, MN, USA. Exclusion criteria: PARTIAL AORTIC OBSTRUCTION PROCEDURE N pregnancy; The device is a multi-lumen catheter with two balloons N large infarct on CT scan (equivalent to 1/3 MCA mounted near its tip, which is designed to partially involvement); obstruct aortic blood flow in a controlled fashion N CT evidence of hydrocephalus sufficient to explain (Figure 1). Patients were treated with 5000 IU of heparin as a bolus, after obtaining a cerebral baseline parench- symptoms; ymography and abdominal angiogram to determine the N intracerebral hematoma not attributable to aneurysm aortic measurement, and optimal device positioning was rupture; obtained (Figure 2A). A catheter balloon was inserted via N NIHSS >15 point; the transfemoral approach, through a 9F introducer N concurrent or intended therapy with coumadin, sheath, over a 0.035-inch guide wire positioned above heparin, thrombolytics or intended therapy with IIb/ and below the renal artery ostia (Figure 2B), and then the IIIa antagonist (periprocedural heparin may be device was secured to the patient’s leg. Several marker administered at the discretion of the interventionalist bands allow radioscopy control during the augmentation. in consultation with the neurologist); The central lumen was connected to a supra-renal blood S130 Neurological Research, 2005, Volume 27, Supplement 1
  3. 3. Partial aortic obstruction: P. Lylyk et al. Figure 2: (A) Aortogram in AP view showing points of measurement (arrows). (B) Device in position. (C) IR balloon inflated at 70%. (D) Both balloons inflated at 70%. (E) Both balloons are deflated pressure monitoring port. The balloons were inflated long as the risk of vasospasm persisted. Changes in Mfv under standard recommendations (Manual inflation were expressed as an increased percentage from base- device, Merritt Medical, UT). Baseline NIHSS score, line value and baseline value was calculated as the Mvf of both MCA by TCD, ECG and MAP were recorded. mean of three consecutive readings. Improved CBF was The infrarenal (IR) balloon was inflated to obstruct 70% assessed by bilateral cerebral DSA obtained in the AP of the aortic lumen (Figure 2C), and then 20 minutes later view following aortic arch injection of 45 ml of the suprarenal (SR) balloon was inflated to obstruct 70% non-ionic contrast solution injected by pump over a of the aortic lumen (Figure 2D). Provision was made to 3-second period; two images per second were obtained reduce the degree of inflation for patients in whom over a 15-second period. We obtained a parenchymo- MAP increased over 30% above the baseline value. graphy at baseline and post-aortic obstruction (Figures 3 The total time of aortic obstruction was 60 minutes. and 4). Either delay of capillary blush or regional Following this period, balloons were sequentially deficit in the capillary phase was defined as a regional deflated over a period not less than 5 minutes for CBF defect. We used a qualitative analysis of circu- each one. With both balloons deflated (Figure 2E), the lation time in one hemisphere to compare with the device was removed and examined. We measured other. DSA at baseline and following balloon deflation diuresis, sensitivity, skin color, movement and pulse in was performed. In addition, the caliber of cerebral both feet, the NIHSS score, Mvf of both MCA by TCD, arteries with vasospasm in segment C5 to A1, M1, V4, B ECG, and intra-arterial and arm MAP after 20 minutes of and P1 were measured in some patients, to compare IR balloon inflation, after 40 and 60 minutes with both with contralateral, uninvolved, or adjacent vessels of balloons inflated and after 20 minutes with both balloons normal caliber, before and following aortic obstruction. deflated. Brain CT scans were made before enrollment and 30 days after treatment. An independent radiologist Pressure monitoring blinded to the clinical patient outcome evaluated all During aortic occlusion, MAP via catheter ports images. above the obstruction and in the arm were monitored. MAP value represented the mean of three consecutive Clinical assessment readings, and it was measured at baseline, at 20, 40 and For a neurological assessment we used the NIHSS, at 60 minutes, and 20 minutes after balloon deflation. baseline, at 20, 40, 60 and 20 minutes after the procedure (or upon awakening if the patient was Adverse events sedated). The same scale was used at 5, 7 and 30 days All adverse events and their relationship to the device after treatment, at the end of follow-up, incapacity was or procedure were recorded. At the end of procedure, measured by mR scale. the device was carefully tested. Statistical analysis ASSESSMENT OF CEREBRAL BLOOD FLOW CHANGES Baseline clinical and demographic information was Augmentation of CBF was assessed by TCD. A 2-MHz summarized as means and standard deviations for pulsed-wave TCD probe was used and MCA was quantitative variables, and as frequencies for categorical insonated. Maximum Mfv over both MCA was recorded data. Formal statistical testing of mean change from at baseline, at 20, 40 and 60 minutes, and 20 minutes baseline in Mfv and NIHSS was achieved via the paired after balloon deflation, and twice a day, every day, as form of Student’s t-test. All p-values are two-sided. Neurological Research, 2005, Volume 27, Supplement 1 S131
  4. 4. Partial aortic obstruction: P. Lylyk et al. Figure 3: Baseline parenchymogram showing a regional perfusion deficit (arrow) RESULTS through the 30-day follow-up period in all but one Twenty-four patients (nine males, 15 females), ranging patient. IR aortic diameter ranged from 11 to 23 mm in age from 30 to 55 years (mean 43), were enrolled At (mean 14.3 mm) and SR ranged from 13.4 to 29 mm the time of SAH the Hunt and Hess grading scale ranged (mean 19.86 mm). Baseline capillary phase on par- from 1 to 4 (mean 2.4), and Fisher score range from 1 to enchymography was abnormal in all patients, including 4 (mean 3.4). Eighteen patients had a single aneurysm delay in wash-in or wash-out of contrast. Regional CBF and six patients had multiple aneurysms. All ruptured defect was observed in 18 patients. Illustrative cases are aneurysms were secured with GDC coils (BSci-Target, shown in Figures 2–4. Parenchymography performed Fremont, Ca). All but one symptomatic aneurysm was after device deflation showed evident improvement of small and all but one was in the anterior circulation. focal perfusion defects in 16 patients. Two of them One patient had a basilar tip aneurysm. Mean onset of returned to normal circulation time with a symmetrical focal neurological symptoms was 9 days (range from interhemispheric capillary phase (Figure 4). There was 4 hours to 15 days) after SAH. Mean time from onset of no change in postprocedural angiography in seven symptomatic vasospasm to treatment ranged from patients, and worsening was seen in one. In six patients, 0.50 minutes to 72 hours. Two patients were treated an increase in vessel caliber was noted at M1, A1 and with Triple H therapy and one patient with volume basilar artery. expansion prior to the procedure for 24 and 72 hours, Mfv increased in all patients. Mean increase from respectively, but showed no improvement. Baseline baseline value in both MCA during the partial obstruc- NIHSS ranged from 2 to 15 points. Twenty patients tion phase was 39% (range from 3 to 147; p50.01), and showed a 2 point or greater reduction in NIHSS score exceeded 15% in 23 patients. In the MCA of the 20 minutes after procedure and 14 patients had symptomatic side, Mfv increased in 23 patients; the >4 points reduction. Mean reduction in NIHSS score mean increase on the symptomatic side was 29% (range following the procedure was 3.4 points (SD 2.9, range 2–73; p50.003). Mvf on the asymptomatic side 0–8 points, p50.005). This response was sustained increased steadily with progressive luminal obstruction, S132 Neurological Research, 2005, Volume 27, Supplement 1
  5. 5. Partial aortic obstruction: P. Lylyk et al. Figure 4: Parenchymogram after procedure showing improvement of focal perfusion defect from 8% during infrarenal balloon inflation to 39% procedure. Sixteen patients had an NIHSS score of during maximal inflation of both balloons. Twenty 2 points or less at 30 days. Three patients died, one of minutes following the procedure, Mfv remained unrelated Staphylococcus aureus sepsis, and two by improved in respect of baseline values in 16 of 24 multiple bilateral brain infarcts due to malignant patients. Mfv was still above baseline value 24 hours vasospasm, refractory to angioplasty and intra-arterial after the procedure in 10 patients. Average increase in nimodipine. MAP above the device at maximal luminal obstruction In 14 patients, CT scan evidence of infarction was was 6% (range 0–20). In one patient, MAP fell by 16% observed before the NeuroFlo procedure. The infarcts during balloon inflation. The restriction on maximal were aisled in eight, and multiple with watershed MAP increase did not limit device inflation in any distribution in six. After the procedure, two patients patient. Mean decrease in arterial blood pressure from developed new territorial infarcts. One patient had a baseline value after balloon deflation was 6% (range focal cortical left frontal paramedian ischemic area prior 0–22). During the procedure, one patient developed to the procedure, which disappeared from the CT at the pain, loss of skin color and pulse in the right foot, on the 30-day follow-up. At 30-day follow-up, three patients side of the device insertion. These symptoms disap- scored 6 points, three patients scored 3 points, six peared with partial deflation of the IR balloon and the patients scored 1 point, and 12 had 0 points in the procedure was halted. Two patients presented agitation modified Rankin scale. during the inflation of IR balloon and required sedation. None of the patients experienced cerebral hemorrhage, or cardiac, mesenteric, spinal or renal complications, CLINICAL CASE (PATIENT 2) during or following the procedure. There were no other A 47-year-old woman with a ruptured posterior com- procedure-related complications. municating artery aneurysm (Hunt–Hess 1, Fisher grade The patient who received Triple-H therapy before the 3) developed stupor, right hemiparesis and aphasia procedure, continued on this treatment following the (NIHSS score 10) 14 days after SAH. DSA showed Neurological Research, 2005, Volume 27, Supplement 1 S133
  6. 6. Partial aortic obstruction: P. Lylyk et al. vasospasm on the left A2 and M2, with a filling regional address blood flow deficits in deep white matter regions. defect over the ipsilateral brain hemisphere on the Nonetheless, it provided a qualitative window to assess parenchymograph. After coiling the aneurysm, the relative circulation time and CBF deficits, before and partial aortic obstruction procedure was performed after NeuroFloTM use. Results with this technique are without complications. At the end of the procedure, affected by contrast injection rates, catheter size, filming aphasia and hemiparesis resolved (NIHSS score 2) and rate, cardiac output and heart rate. However, we felt the parenchymograph returned to normal. Mfv controlling for differences in these variables was increased 23% from baseline value on the symptomatic inconsequential in our patient group. side, and MAP was stable throughout. The patient The significance of the Mfv by TCD changes during remained well after the procedure and mR scored was the treatment of vasospasm is interesting, since mean zero at 30 days. (Figures 3 and 4) flow velocity is inversely proportional to vessel dia- meter, reducing diameter increases flow. In patients with vasospasm, increases of velocity are indicative of a DISCUSSION progressive reduction in vessel diameter, with the CBF brain defects are very common after SAH. The possibility of crossing a critical limit in flow reduction prevalence of CBF abnormalities among symptomatic and the appearance of clinical symptoms. When mean patients is roughly the same as it is for asymptomatic flow velocity is augmented due to vasospasm and blood patients11,12, and ranges from 64% by magnetic volume increases, blood flow velocity increases without resonance perfusion imaging, to 82% by SPECT11. a reduction of the vascular caliber. Therefore, an The ability of the brain tissue to tolerate oligohemia increase of mean flow velocity can be interpreted as a depends on several factors, e.g. blood pressure, condition of either worsening or improvement, accord- hemoglobin concentration, degree of flow reduction ing to the factors we mentioned above. and tissue oxygen demands. In all of these conditions, Significant velocity increases detected contralateral to collateral brain circulation plays an important role. At a the ischemic hemisphere within seconds of balloon critical threshold, symptoms develop and progress to inflation and progressive augmentation with increasing infarction, unless CBF can be improved. Several levels of aortic obstruction, certainly suggest that CBF therapeutic regimens for vasospasm have been shown has improved. Furthermore, increases in velocity were to be beneficial. Using Xenon to determine regional paralleled by symptomatic improvement in many cases. cerebral blood flow, a 14% global CBF increase was However, if vessel caliber increases, one can no longer demonstrated within 60 minutes of oral or intravenous assume that an increase in velocity reflects a corre- nimodipine administration in 11 patients with SAH and sponding change in cerebral blood flow. Dilatation of in six patients with symptomatic vasospasm. CBF the basal arteries during angioplasty, for example, is improvement was most pronounced in the regions with associated with decreases in velocity, with or without most decreased flow before treatment13. In another an increase in CBF, while lesser degrees of dilatation study involving 10 patients with symptomatic vasos- using papaverine have been associated with an increase pasm undergoing angioplasty, SPECT scans showed in cerebral flow16,17. increase perfusion in nine of 10 patients, of whom eight At least in some instances, aortic obstruction (80%) also improved clinically. The average of increase increases proximal vessel caliber and velocities in the in the CBF in patients with clinical improvement was in non-ischemic hemisphere. The mechanism by which the order of 10%5. Recently, using thermal diffusion partial aortic obstruction augments cerebral perfusion flowmetry, the administration of intra-arterial papaver- has not been established. Anecdotal reports indicate ine to symptomatic patients was also found to produce a that patients with vasospasm and poor cardiac function significant, albeit very short-lived, increase in cerebral improve during treatment with intra-aortic balloon blood flow14. counter-pulsation, and the improvement has been attri- The effect of these therapeutic modalities on clinical buted to an increase in cardiac output and MAP18–20. outcome has not yet been studied in a systematic This is unlikely to be the mechanism in our patients fashion. In the present study, we document regional since cardiac function was normal. We have previously improvements in CBF by angiographic images in 16 of reported that, in a swine model, aortic obstruction 24 patients following treatment with transitory partial using the NeuroFlo device did not affect cardiac output aortic obstruction. In our unpublished experience, over a 2-hour period21. Hypertension is only a minor parenchymography is a method of qualitatively asses- contributor to the improved cerebral flow achieved sing CBF, as demonstrated by Iseda et al. in a study of using the device, since the mean increase in MAP was seven patients with symptomatic vasospasm, In this only 6%. This is quite different to what is observed in study there was a strong relationship between angio- patients treated with pharmacological induced hyper- graphic and SPECT changes15. As only an anterior- tension. In a recent study involving 19 patients with posterior view on cerebral angiography following aortic ischemic stroke, hypervolemic, hypertensive therapy arch injection was obtained, more regional improve- was associated with a 30% increase in MAP, but only a ments in distal territories may have been overlooked 17% increase in contralateral cerebral blood flow22. due to superimposition of images. Indeed, this techni- Controlled aortic obstruction by balloon catheter que was chosen as a crude measure of relative cerebral appears to be safe in patients with symptomatic blood flow. It was not quantitative and could not vasospasm once the aneurysm is secured. Cardiac S134 Neurological Research, 2005, Volume 27, Supplement 1
  7. 7. Partial aortic obstruction: P. Lylyk et al. failure, cerebral edema and even cerebral hemorrhage, 5 Barnwell SL, Higashida RT, Halbach VV, et al. Transluminal angioplasty of intracerebral vessels for cerebral arterial spasm: which frequently complicate hypertensive therapy, did reversal of neurological deficits after delayed treatment. not occur in any of our patients. Limb ischemia Neurosurgery 1989; 25: 424–427 developed in one patient, but decreased immediately 6 Higashida RT, Halbach VV, Dowd CF, et al. Intravascular balloon after partial deflation of the infrarenal balloon. Reducing dilation therapy for intracranial arterial vasospasm: patient the sheath size may reduce the likelihood of this selection, technique, and clinical results. Neurosurgery 1992; 15: 89–95 complication to occur. 7 Andaluz N, Tomsick TA, Tew JM Jr, et al. Indications for Symptomatic improvement in the majority of patients endovascular therapy for refractory vasospasm after aneurysmal was evident during the 1 hour procedure, and was subarachnoid hemorrhage: experience at the University of sustained in all but one patient. The decision to limit the Cincinnati. Surg Neurol 2002; 58: 131–138; discussion 138 treatment to sixty minutes in a feasibility study is based 8 Rajendran JG, Lewis DH, Newell DW, et al. Brain SPECT used to evaluate vasospasm after subarachnoid hemorrhage: correlation upon experimental results. In a rat stroke model, 1 hour with angiography and transcranial Doppler. Clin Nucl Med 2001; of aortic obstruction was associated with a 67% 26: 125–130 reduction in infarct volume at 48 hours (unpublished 9 Naderi S, Ozguven MA, Bayhan H, et al. Evaluation of cerebral results). In future studies, if patients deteriorate follow- vasospasm in patients with subarachnoid hemorrhage using single photon emission computed tomography. Neurosurg Rev 1994; 17: ing initial treatment, retreatment may prove to be 261–265 valuable. Leaving the sheath in at the end of the 10 Leclerc X, Fichten A, Gauvrit JY, et al. Symptomatic vasospasm procedure, possibly overnight, would simplify this after subarachnoid hemorrhage: assessment of brain damage by process. The impact of this new treatment modality on diffusion and perfusion-weight MRI and single photon emission long-term outcome remains to be determined. computed tomography. Neuroradiology 2002; 44: 610–616 11 Hosono M, Machida K, Matsui T, et al. Non-invasive quantitative Historically, the incidence of stroke and death in monitoring of cerebral blood flow in aneurysmal subarachnoid patients with symptomatic vasospasm has been reported hemorrhage with 99mTc-ECD. Nucl Med Commun 2002; 23: 5– to be as high as 60%23, especially among those with CT 11 evidence of infarction at the time of diagnosis. Among 12 Gaab MR, Haubitz I, Brawanski A, et al. Acute effects of nimodipine on the cerebral blood flow and intracranial pressure. patients with symptomatic vasospasm, 46% were found Neurochir (Stuttg) 1985; 28(Suppl 1): 93–99 to have poor outcome. In our study, 18 of 24 (75%) 13 Vajkoczy P, Horn P, Bauhuf C, et al. Effect of intra-arterial patients had good outcome. papaverine on regional cerebral blood flow in hemodynamically relevant cerebral vasospasm. Stroke 2001; 32: 498–505 14 Iseda T, Nakano S, Yoneyama T, et al. Angiographic cerebral CONCLUSIONS circulation time before and after endovascular therapy for We have showed, in patients with symptomatic symptomatic vasospasm. Clin Radiol 2000; 55: 679–683 15 Oskouian RJ Jr, Martin NA, Lee JH, et al. Multimodal quantitation vasospasm, that partial and transitory aortic obstruction of the effects of endovascular therapy for vasospasm on cerebral using the NeuroFloTM device was safe and technically blood flow, transcranial Doppler ultrasonographic velocities, and simple. This novel method of treatment improves cerebral artery diameters. Neurosurgery 2002; 51: 30–41; discus- clinical outcome in 75% of patients and increases sion 41–43 cerebral blood flow without inducing significant hyper- 16 Apostolides PJ, Greene KA, Zabramski JM, et al. Intra-aortic balloon pump counterpulsation in the management of concomi- tension. Further studies are required to improve the tant cerebral vasospasm and cardia failure after subarachnoid level of evidence of efficacy in a randomized study. hemorrhage: technical case report. Neurosurgery 1996; 38: 1056– 1059, discussion 1059–1060 17 Nussbaum ES, Sebring LA, Ganz WF, et al. Intra-aortic balloon ACKNOWLEDGEMENTS counterpulsation augments cerebral blood flow in the patient with We thank Dr Robin Roberts for assistance with the statistical analysis and cerebral vasospasm: a xenon-enhanced computed tomography Dr Song for analysing images and TCDs. study. Neurosurgery 1998; 42: 206–211 18 Rosen CL, Sekhar LN, Duong DH. 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