Intra-arterial nicardipine infusion improves CT perfusion-measured cerebral blood flow in patients with subarachnoid hemorrhage-induced vasospasm.
ABSTRACT Our aim was to determine the effects of intra-arterial (IA) nicardipine infusion on the cerebral hemodynamics of patients with aneurysmal subarachnoid hemorrhage (aSAH)-induced vasospasm by using first-pass quantitative cine CT perfusion (CTP).
Six patients post-aSAH with clinical and transcranial Doppler findings suggestive of vasospasm were evaluated by CT angiography and CTP immediately before angiography for possible vasospasm treatment. CTP was repeated immediately following IA nicardipine infusion. Maps of mean transit time (MTT), cerebral blood volume (CBV), and cerebral blood flow (CBF) were constructed and analyzed in a blinded manner. Corresponding regions of interest on these maps from the bilateral middle cerebral artery territories and, when appropriate, the bilateral anterior or posterior cerebral artery territories, were selected from the pre- and posttreatment scans. Normalized values were compared by repeated measures analysis of variance.
Angiographic vasospasm was confirmed in all patients. In 5 of the 6 patients, both CBF and MTT improved significantly in affected regions in response to nicardipine therapy (mean increase in CBF, 41 +/- 43%; range, -9%-162%, P = .0004; mean decrease in MTT, 26 +/- 24%; range, 0%-70%, P = .0002). In 1 patient, we were unable to quantify improvement in flow parameters due to section-selection differences between the pre- and posttreatment examinations.
IA nicardipine improves CBF and MTT in ischemic regions in patients with aSAH-induced vasospasm. Our data provide a tissue-level complement to the favorable effects of IA nicardipine reported on prior angiographic studies. CTP may provide a surrogate marker for monitoring the success of treatment strategies in patients with aSAH-induced vasospasm.
- SourceAvailable from: jackmd.com[show abstract] [hide abstract]
ABSTRACT: Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). It is associated with high morbidity and mortality rates, even after the aneurysm has been secured surgically or radiologically. A great deal of experimental and clinical research has been conducted in an effort to find ways to prevent this complication. The literature includes extensive coverage of in vivo animal model studies of SAH and vasospasm. These experimental studies have contributed to tremendous advances in the understanding of the mechanisms leading to cerebral vasospasm. Most of the experimental settings, however, have demonstrated varying levels of ability to predict accurately what occurs in human SAH. Therefore, although animal models have been developed to test new therapies, most of the treatment effects have been shown to be less compelling when trials have been conducted in clinical settings. The interpretation of current literature is complicated further by the imprecise estimation of the incidence of cerebral vasospasm, which is due to various degrees of clinical expression, ranging from the absence of symptoms in the presence of increased blood flow velocities at transcranial Doppler or vessel diameter reduction at angiography to neurological manifestations of severe ischemic deficits. In addition, a change over time in the incidence pattern of human SAH and vasospasm, possibly related to improved surgical techniques and overall patient management, may have occurred. This topic review collects the relevant literature on clinical trials investigating prophylactic therapies for cerebral vasospasm in patients with aneurysmal SAH and emphasizes the need for large clinical trials to confirm the results derived from clinical experience. In addition, it points out some experimental therapies that may hold promise in future clinical trials to prevent the occurrence of vasospasm.Neurosurgery 03/2001; 48(2):249-61; discussion 261-2. · 2.53 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: The reduction in the level of nitric oxide (NO) is a purported mechanism of delayed vasospasm after subarachnoid hemorrhage (SAH). Evidence in support of a causative role for NO includes the disappearance of nitric oxide synthase (NOS) from the adventitia of vessels in spasm, the destruction of NO by hemoglobin released from the clot into the subarachnoid space, and reversal of vasospasm by intracarotid NO. The authors sought to establish whether administration of L-arginine, the substrate of the NO-producing enzyme NOS, would reverse and/or prevent vasospasm in a primate model of SAH. The study was composed of two sets of experiments: one in which L-arginine was infused over a brief period into the carotid artery of monkeys with vasospasm, and the other in which L-arginine was intravenously infused into monkeys over a longer period of time starting at onset of SAH. In the short-term infusion experiment, the effect of a 3-minute intracarotid infusion of L-arginine (intracarotid concentration 10(-6) M) on the degree of vasospasm of the right middle cerebral artery (MCA) and on regional cerebral blood flow (rCBF) was examined in five cynomolgus monkeys. In the long-term infusion experiment, the effect of a 14-day intravenous infusion of saline (control group, five animals) or L-arginine (10(-3) M; six animals) on the occurrence and degree of cerebral vasospasm was examined in monkeys. The degree of vasospasm in all experiments was assessed by cerebral arteriography, which was performed preoperatively and on postoperative Days 7 (short and long-term infusion experiments) and 14 (long-term infusion experiment). In the long-term infusion experiment, plasma levels of L-arginine were measured at these times in the monkeys to confirm L-arginine availability. Vasospasm was not affected by the intracarotid infusion of L-arginine (shown by the reduction in the right MCA area on an anteroposterior arteriogram compared with preoperative values). However, intracarotid L-arginine infusion increased rCBF by 21% (p < 0.015; PCO2 38-42 mm Hg) in all vasospastic monkeys compared with rCBF measured during the saline infusions. In the long-term infusion experiment, vasospasm of the right MCA occurred with similar intensity with or without continuous intravenous administration of L-arginine on Day 7 and had resolved by Day 14. The mean plasma L-arginine level increased during infusion from 12.7+/-4 microg/ml on Day 0 to 21.9+/-13.1 microg/ml on Day 7 and was 18.5+/-3.1 microg/ml on Day 14 (p < 0.05). Brief intracarotid and continuous intravenous infusion of L-arginine did not influence the incidence or degree of cerebral vasospasm. After SAH, intracarotid infusion of L-arginine markedly increased rCBF in a primate model of SAH. These findings discourage the use of L-arginine as a treatment for vasospasm after SAH.Journal of Neurosurgery 01/2000; 92(1):121-6. · 3.15 Impact Factor
- Journal of Head Trauma Rehabilitation - J HEAD TRAUMA REHABIL. 01/1990; 5(3):75-77.
Intra-Arterial Nicardipine Infusion Improves CT
Perfusion–Measured Cerebral Blood Flow in
Patients with Subarachnoid Hemorrhage–Induced
BACKGROUND AND PURPOSE: Our aim was to determine the effects of intra-arterial (IA) nicardipine
infusion on the cerebral hemodynamics of patients with aneurysmal subarachnoid hemorrhage
(aSAH)–induced vasospasm by using first-pass quantitative cine CT perfusion (CTP).
MATERIALS AND METHODS: Six patients post-aSAH with clinical and transcranial Doppler findings
suggestive of vasospasm were evaluated by CT angiography and CTP immediately before angiography
for possible vasospasm treatment. CTP was repeated immediately following IA nicardipine infusion.
Maps of mean transit time (MTT), cerebral blood volume (CBV), and cerebral blood flow (CBF) were
constructed and analyzed in a blinded manner. Corresponding regions of interest on these maps from
the bilateral middle cerebral artery territories and, when appropriate, the bilateral anterior or posterior
cerebral artery territories, were selected from the pre- and posttreatment scans. Normalized values
were compared by repeated measures analysis of variance.
RESULTS: Angiographic vasospasm was confirmed in all patients. In 5 of the 6 patients, both CBF and
MTT improved significantly in affected regions in response to nicardipine therapy (mean increase in
CBF, 41 ? 43%; range, ?9%–162%, P ? .0004; mean decrease in MTT, 26 ? 24%; range, 0%–70%,
P ? .0002). In 1 patient, we were unable to quantify improvement in flow parameters due to
section-selection differences between the pre- and posttreatment examinations.
CONCLUSIONS: IA nicardipine improves CBF and MTT in ischemic regions in patients with aSAH-
induced vasospasm. Our data provide a tissue-level complement to the favorable effects of IA
nicardipine reported on prior angiographic studies. CTP may provide a surrogate marker for monitoring
the success of treatment strategies in patients with aSAH-induced vasospasm.
deed, the presence of cerebral vasospasm has been associated
with a 1.5 to threefold increase in mortality during the first 2
patients with aSAH die from vasospasm.1,2According to the
Cooperative Aneurysm Study, 70% of the patients who
present with aSAH develop vasospasm, with symptomatic
brain ischemia or infarcts occurring in 36% of all patients.3
the management of patients with aSAH is the prevention, de-
tection, and treatment of vasospasm. The most commonly
used approaches include oral nimodipine; induced hyperten-
sion, hemodilution, and hyperdynamic (triple-H) therapy;
and endovascular techniques, including intra-arterial (IA) in-
elayed cerebral ischemia represents one of the leading
causes of morbidity and mortality in patients with aneu-
gioplasty (PTA), or a combination of the 2.
Given its short duration of action and several potential
complications, papaverine has been largely replaced by other
dene IV),6or nimodipine7as the drug of choice for IA vaso-
the primary endovascular vasospasm treatment at our hospi-
tal. Nicardipine is known to affect positively both angio-
graphic (increasing vessel diameter) and clinical vasospasms.6
The degree to which nicardipine actually augments tissue-
level perfusion, however, has not, to our knowledge, been
evaluation of patients with clinically significant aSAH-in-
duced vasospasm has been previously demonstrated.8-11The
IA nicardipine infusion on the cerebral hemodynamics of pa-
tients with aSAH-induced vasospasm as measured by first-
esis that CTP may be a useful tool in the quantification of the
future clinical trials.
Materials and Methods
aSAH between September 2002 and June 2004. Approval was ob-
tained from the institutional review board at our institution to con-
Received March 28, 2008; accepted after revision July 11.
From the Endovascular Neurosurgery/Interventional Neuroradiology Section, Departments
of Radiology and Neurosurgery (R.G.N., J.A.H., J.D.R., J.C.P.); Neurocritical Care and
Vascular Neurology Section, Department of Neurology (R.G.N., G.A.R.); Diagnostic Neuro-
radiology Section, Department of Radiology (M.H.L., L.R., R.G.G., E.F.H.); Vascular Neuro-
surgery Section, Department of Neurosurgery (C.S.O.), Massachusetts General Hospital,
Harvard Medical School, Boston, Mass.
Paper previously presented in part at: Annual Meeting of the American Society of
Neuroradiology, June 5–11, 2004; Seattle, Wash.
Please address correspondence to Raul G. Nogueira, MD, Department of Interventional
Neuroradiology and Endovascular Neurosurgery, Massachusetts General Hospital, 55 Fruit
St, GRB-2-241, Boston, MA, 02114; e-mail: RNOGUEIRA@PARTNERS.ORG
Nogueira ? AJNR 30 ? Jan 2009 ? www.ajnr.org
duct this retrospective review. Informed consent for endovascular
treatment was obtained as part of routine clinical care. All patients
with aSAH are treated under a standard protocol, which includes
admission to the neuroscience intensive care unit for preoperative
and postoperative monitoring. After surgical or endovascular treat-
ment of the aneurysm, patients are routinely maintained in a rela-
tively hypertensive and euvolemic state in anticipation of cerebral
vasospasm. Daily clinical observations and transcranial Doppler
(TCD) measurements are used to detect vasospasm. Patients with
TCD findings suggestive of vasospasm are typically treated with in-
duced hypertension (with phenylephrine and/or norepinephrine)
and hypervolemia (crystalloids ? albumin to maintain central ve-
nous pressure above 12 mm Hg).
CT angiography (CTA) and concomitant first-pass quantitative
cine CTP are typically performed in patients with clinical findings
reliable neurologic assessment cannot be obtained (eg, intubated pa-
the CTA and/or CTP, then IA vasodilation with nicardipine and/or
PTA are typically used. A retrospective review of our aSAH data base
and right after undergoing vasospasm treatment with IA nicardipine
CTP scans. These 6 patients are the subjects of this study.
CT was performed by using a multidetector (16 sections) helical CT
scanner (LightSpeed; GE Healthcare, Milwaukee, Wis) in the head-
first supine orientation. An 18-gauge cannula was placed into an an-
tecubital vein before the patient’s entry into the scanner. Once in the
pump was connected to the cannula. A precontrast axial study was
obtained from the foramen magnum to the vertex. Immediately fol-
mL/s (Omnipaque, 300 mg I/mL; Amersham Health, Princeton, NJ).
The imaging parameters used during this phase were 140 kilovolt
(peak) (kV[p]), 170 mA, 0.8-second rotation time, 2.5-mm section
thickness, 512 ? 512 image matrix, and standard algorithm recon-
struction. Maximal attenuation projection and 3D images were then
constructed by using GE Healthcare and Vitrea (Vital Images,
Minnetonka, Minn) workstations.
istration of 50 mL of iodinated contrast material by using the same
intravenous route at 7 mL/s with a 5-second delay. The imaging pa-
rameters used were 80 kV(p), 200 mA, 1-second rotation time, 4
per section, 5-mm section thickness, 512 ? 512 image matrix, and
selected from axial cuts of the supraclinoid internal carotid artery
(ICA) or the A2 segment of the anterior cerebral artery (ACA).12The
same AIF was used for both pre- and posttreatment studies. CTP
images were obtained just before and immediately after the endovas-
Endovascular Treatment Protocol
Digital subtraction angiography (DSA) was performed by use of the
transfemoral Seldinger technique. Once vasospasm was confirmed,
0.1 mg/mL and administered in 1-mL aliquots through a Prowler
microcatheter (Cordis Neurovascular, Miami Lakes, Fla) into the af-
imal basilar artery). All patients had a ventriculostomy catheter. If
ventriculostomy was opened and allowed to drain to lower the ICP.
Continuous blood pressure monitoring was also available in all pa-
tients through a radial arterial line. Cerebral perfusion pressure was
maintained above 70 mm Hg throughout the procedure.
Data Processing and Analysis
(Advantage Windows; GE Healthcare) and analyzed with commer-
cially available perfusion analysis software (CT Perfusion-2 software,
FuncTool 3.0; GE Healthcare) to create maps of mean transit time
(MTT), cerebral blood volume (CBV), and cerebral blood flow
The CBF, CBV, and MTT data were transferred to a personal
computer for analysis. Regions of interest were outlined by using a
the CTA and angiographic procedure results. One slab for each terri-
tory on each scan was selected on the basis of the levels that looked
most comparable between the pre- and posttreatment scans. Region-
of-interest contours were delineated in the bilateral middle cerebral
ment perfusion maps. The regions of interest were copied on the
anatomically corresponding locations on the posttreatment CTP
maps. For each region, mean pre- and posttreatment CBF, CBV, and
MTT values were calculated.
The relative rate of change (eg, percentage change in the posttreat-
ment values when compared with the pretreatment values) in CBF,
Comparison of pretreatment with posttreatment changes in CBF,
variance with the patient as a fixed effect and pre- and posttreatment
computations were performed with the aid of SAS software (Version
9.1; SAS Institute, Cary, NC).
aSAH, age, sex, Hunt and Hess grade, Fisher group, location
and treatment of the aneurysm, location and severity of the
vasospasm, IA nicardipine dosage per location, and pre- and
posttreatment CTP data are summarized in the Table.
A total of 15 vessels were successfully treated in 6 patients.
One patient underwent PTA in addition to IA nicardipine in-
fusion. The remaining patients were treated only with IA ni-
cardipine. The total dose ranged from 6 to 30 mg per patient.
In 1 patient, we were unable to quantify improvement in flow
parameters, due to section-selection differences between the
pre- and posttreatment CTP examinations. This patient was
not included in our quantitative analysis; however, subjective
analysis of the 2 closest pre- and posttreatment sections was
suggestive of posttreatment improvement.
A total of 16 vascular territories were analyzed in the re-
AJNR Am J Neuroradiol 30:160–64 ? Jan 2009 ? www.ajnr.org
ries in 2 patients, bilateral MCA and PCA territories in 1 pa-
tient, and bilateral MCA territories in 2 patients. One patient
mg of nicardipine infusion in the right ICA, resulting in only
minimal angiographic response. In another patient (case 5),
only the left ICA was treated because the procedure had to be
aborted due to seizures. In the remaining 14 vascular territo-
ries, treatment resulted in satisfactory angiographic response.
Both CBF and MTT improved significantly in the affected
regions in response to IA nicardipine therapy. Mean CBF in-
creased from 38.2 ? 13.1 mL/100 g/min in the pretreatment
CTP scan to 50.7 ? 12.9 mL/100 g/min in the posttreatment
1.3 seconds in the posttreatment CTP scan, resulting in a rel-
ative MTT reduction of 26.2 ? 24.2% (range, 0%–70%; P ?
pretreatment CTP scan and 2.9 ? 0.8 mL/100 g in the post-
?44%–34%; P ? .63). Fig 1 illustrates the effects of IA nicar-
dipine infusion on DSA and MTT maps.
To assess the possibility that the aforementioned benefit
was mostly related to PTA, we performed a second analysis
excluding the 4 vascular territories (case 2) that were also
ics remained statistically significant, with a relative CBF in-
crease of 25.7 ? 25.9% (range, ?9%–69%; P ? .01) and a
In the present study, we have described the direct effects of IA
nicardipine on reduced CBF in patients with hemodynami-
cally significant vasospasm after aSAH by using first-pass
1) the characterization of the acute CBF response to IA nicar-
dipine infusion; and 2) the validation of the use of CTP in the
assessment of new treatment modalities for vasospasm.
The mechanism by which aSAH-induced vasospasm oc-
curs is not yet fully understood; however, both experimental
and clinical data strongly suggest the efficacy of calcium an-
tagonists in the treatment and prevention of vasospasm.13-15
Nimodipine, an oral dihydropyridine calcium antagonist, has
been shown to reduce the incidence of vasospasm-induced
cerebral infarction by 34% and the rate of poor outcomes by
40%.16Nicardipine is another dihydropyridine calcium an-
tagonist, which has more selective effects on vascular smooth
muscle than on cardiac muscle. Several studies have demon-
strated that continuous intravenous nicardipine infusion sig-
nificantly decreases the incidence of symptomatic, angio-
graphic, and TCD vasospasm.15,17,18However, the efficacy of
monary edema, and renal dysfunction.
Badjatia et al6have previously demonstrated that IA nicar-
dipine infusion improves angiographic vasospasm with an ef-
fect more sustained than what has been reported with papav-
ment as demonstrated by the lack of correlation between an-
giographic and clinical improvement in many situations. For
instance, patients treated with IA papaverine may still have
further neurologic deterioration despite angiographic im-
Patient data summary
10 mg, R ICA
10 mg, L ICA
10 mg, BA
2.0424 44F33 L ACA,
4 mg, R ICA
R ACASeverePTA, R ICA
PTA, R M1
4 mg, L ICA
PTA, L ICA
2 mg, L A1
PTA, L A1
4 mg R ICA
31155F23 No aneurysm
R MCAModerate4.794.44 45.2656.112.793.38
2 mg, R A1
4 mg, L ICA
2 mg L M2
8 mg, R ICA
6 mg, L ICA
45 44F33BA, clipping
5 11 42M23 AcomA,
L MCAModerate7.5 mg, L ICA5.324.2768.2073.734.714.32
Note:—HH indicates Hunt and Hess; Rx, treatment; R, right; L, left; BA, basilar artery; Mod/sev, moderate to severe; AcomA, anterior communicating artery; MTT, mean transit time; CBF,
cerebral blood flow; CBV, cerebral blood volume; ACA, anterior cerebral artery; MCA, middle cerebral artery; PCA, posterior cerebral artery; ICA, internal carotid artery.
* Near-complete occlusion of the M2 segment of the right MCA on angiographic evaluation with only minimal angiographic response after IA nicardipine infusion.
† Procedure aborted due to seizures.
Nogueira ? AJNR 30 ? Jan 2009 ? www.ajnr.org
may demonstrate remarkable clinical improvement despite
L-arginine has been shown to markedly increase CBF in a pri-
mate model of SAH, despite the lack of any angiographic
changes.20Changes in perfusion at the microvasculature level
probably account for this clinicoangiographic dissociation.
Therefore, assessment of cerebral perfusion as opposed to an-
novel therapies for vasospasm.
As an example, Firlik et al19have demonstrated that IA
papaverine may fail to improve CBF despite reversal of angio-
graphic vasospasm. These authors reported a series of 15 pa-
tients with symptomatic vasospasm who underwent a total of
reversed following treatment on 18 of 23 occasions (78%).
Associated clinical improvement was major on 6 occasions,
but either minor or none on 17. Pre- and posttreatment CBF
was assessed by stable xenon-enhanced CT on 13 occasions
6 of these (46%).19
CTP has been shown to be a useful tool in the selection of
proper candidates for acute stroke thrombolysis21and has
more recently been used to diagnose and guide medical and
endovascular therapy in patients with delayed cerebral isch-
emia after aSAH.8,9,22The application of CTP to assess the
response to vasospasm treatment has also been previously re-
ported. Ono et al23performed CTP in 8 patients with aSAH-
induced vasospasm before, immediately after, and 4.5–6
hours after IA infusion of fasudil hydrochloride with an aver-
cluded that, though initially effective, fasudil hydrochloride is
a short-lived treatment for vasospasm.23In our study, pre-
treatment and immediately posttreatment mean CBF was
38.2 ? 13.1 and 50.7 ? 12.9 mL/100 g/min, respectively.
Our analysis is somewhat limited by its overall small sam-
ple size and by the fact that PTA was performed in 1 of our
patients, and differences in section selection did not allow the
inclusion of that last patient in the analysis. In addition, our
in increasing CBF in patients with vasospasm, we did not as-
Fig 1. Panels 1, 2, and 3 illustrate cases 1, 2, and 3, respectively. Panels A–D show pre- and posttreatment angiograms and MTT maps, respectively. Panel 1: A, Severe vasospasm of
the left PCA, which had a marked response to nicardipine infusion in the basilar artery (1B) resulting in 28% reduction in MTT (1C, -D) and 62% increase in CBF (not shown) at the left
PCA territory. Panel 2: A, Severe vasospasm of the left ACA, which had a marked response to PTA of the A1 segment and nicardipine infusion (2B), resulting in 68% reduction in MTT
(2C, -D) and 89% increase in CBF (not shown) at the left ACA territory. Panel 3: A, Moderate vasospasm of the left MCA, which had only a mild angiographic response to nicardipine
infusion (3B). C and D, Despite the suboptimal angiographic result, there was a 37% reduction in MTT and 69% increase in CBF (not shown) at the left MCA territory. This likely reflects
the nicardipine effect in the microcirculation.
AJNR Am J Neuroradiol 30:160–64 ? Jan 2009 ? www.ajnr.org
sess the duration of this effect due to concerns about the ad-
ditional contrast and radiation exposure that would be neces-
sary for another CTP examination. Despite these limitations,
ment in CBF and MTT immediately after IA nicardipine
IA nicardipine infusion improves CBF and MTT in ischemic
regions in patients with aSAH-induced vasospasm. Our data
able effects of IA nicardipine seen with angiographic studies.
In addition, this study reinforces that CTA/CTP is a safe and
promising technique for the evaluation of aSAH-induced va-
sospasm. Indeed, quantitative CTP may provide a surrogate
marker for monitoring the success of treatment strategies in
patients with aSAH-induced vasospasm. Future studies with
larger sample sizes are required to confirm our results and to
answer the questions about the duration of the treatment ef-
fect as well as its overall impact in clinical outcomes.
1. Macdonald RL, Weir B. Epidemiology. In: Macdonald RL, Weir B. Cerebral
Vasospasm. San Diego, Calif: Academic Press; 2001:16–18
2. Treggiari-Venzi MM, Suter PM, Romand JA. Review of medical prevention of
vasospasm after aneurysmal subarachnoid hemorrhage: a problem of neu-
rointensive care. Neurosurgery 2001;48:249–61, discussion 261–42
3. Adams HP Jr, Kassell NF, Torner JC, et al. Predicting cerebral ischemia after
aneurysmal subarachnoid hemorrhage: influences of clinical condition, CT
results, and antifibrinolytic therapy—a report of the Cooperative Aneurysm
Study. Neurology 1987;37:1586–91
4. Arakawa Y, Kikuta K, Hojo M, et al. Milrinone for the treatment of cerebral
vasospasm after subarachnoid hemorrhage: report of seven cases. Neurosur-
gery 2001;48:723–28, discussion 728–30
5. Feng L, Fitzsimmons BF, Young WL, et al. Intraarterially administered vera-
pamil as adjunct therapy for cerebral vasospasm: safety and 2-year experi-
ence. AJNR Am J Neuroradiol 2002;23:1284–90
6. Badjatia N, Topcuoglu MA, Pryor JC, et al. Preliminary experience with intra-
7. Biondi A, Ricciardi GK, Puybasset L, et al. Intra-arterial nimodipine for the
treatment of symptomatic cerebral vasospasm after aneurysmal subarach-
noid hemorrhage: preliminary results. AJNR Am J Neuroradiol 2004;25:
8. Nogueira RG, Hunter G, Lev MH, et al. Preliminary Data on CT Perfusion in
of the Sixth Joint Annual Meeting of the AANS/CNS Section on Cerebrovascular
Phoenix, Az, 15–19 February 2003.
plication of an existent technique. Neurosurgery 2005;56:304–17, discussion
10. Wintermark M, Ko NU, Smith WS, et al. Vasospasm after subarachnoid
hemorrhage: utility of perfusion CT and CT angiography on diagnosis and
management. AJNR Am J Neuroradiol 2006;27:26–34
11. Sviri GE, Mesiwala AH, Lewis DH, et al. Dynamic perfusion computerized
tomography in cerebral vasospasm following aneurysmal subarachnoid
hemorrhage: a comparison with technetium-99m-labeled ethyl cysteinate
dimer-single-photon emission computerized tomography. J Neurosurg 2006;
12. Sanelli PC, Lev MH, Eastwood JD, et al. The effect of varying user-selected
input parameters on quantitative values in CT perfusion maps. Acad Radiol
13. Alabadi JA, Salom JB, Torregrosa G, et al. Changes in the cerebrovascular ef-
fects of endothelin-1 and nicardipine after experimental subarachnoid hem-
orrhage. Neurosurgery 1993;33:707–14, discussion 714–15
14. Takayasu M, Suzuki Y, Shibuya M, et al. The effects of HA compound calcium
antagonists on delayed cerebral vasospasm in dogs. J Neurosurg 1986;65:
15. Haley EC Jr, Kassell NF, Torner JC, et al. A randomized trial of two doses of
nicardipine in aneurysmal subarachnoid hemorrhage: a report of the Coop-
erative Aneurysm Study. J Neurosurg 1994;80:788–96
bral infarction and outcome after subarachnoid haemorrhage: British aneu-
rysm nimodipine trial. BMJ 1989;298:636–42
intravenous nicardipine in aneurysmal subarachnoid hemorrhage: a report
of the Cooperative Aneurysm Study. J Neurosurg 1993;78:537–47
18. Haley EC Jr, Kassell NF, Torner JC. A randomized trial of nicardipine in sub-
arachnoid hemorrhage: angiographic and transcranial Doppler ultrasound
results—a report of the Cooperative Aneurysm Study. J Neurosurg 1993;78:
19. Firlik KS, Kaufmann AM, Firlik AD, et al. Intra-arterial papaverine for the
rhage. Surg Neurol 1999;51:66–74
reversal or prevention of vasospasm in response to L-arginine infusion after
subarachnoid hemorrhage J Neurosurg 2000;92:121–26
21. Wintermark M, Reichhart M, Thiran JP, et al. Prognostic accuracy of cerebral
blood flow measurement by perfusion computed tomography, at the time of
emergency room admission, in acute stroke patients. Ann Neurol 2002;51:
22. Nabavi DG, LeBlanc LM, Baxter B, et al. Monitoring cerebral perfusion after
subarachnoid hemorrhage using CT. Neuroradiology 2001;43:7–16
23. Ono K, Shirotani T, Wada K, et al. Intra-arterial administration of fasudil
hydrochloride: duration of action [in Japanese]. No Shinkei Geka 2005;33:
Nogueira ? AJNR 30 ? Jan 2009 ? www.ajnr.org