Cerebral Circulation Time Research Articles

Stenotic Transverse Sinus Predisposes to Poststenting Hyperperfusion Syndrome as Evidenced by Quantitative Analysis of Peritherapeutic Cerebral Circulation Time

Hyperperfusion syndrome is a devastating complication of carotid stent placement. The shortening of cerebral circulation time after stent placement is seen as a good indicator of the development of hyperperfusion syndrome. The purpose of our study was to evaluate whether patients with ipsilateral transverse sinus stenosis are prone to having shortened cerebral circulation time after stent placement, subsequently leading to the possible development of hyperperfusion syndrome. Forty-nine patients with >70% unilateral carotid stenosis undergoing stent placement were recruited for analysis. Group A consisted of patients with a stenotic ipsilateral transverse sinus >50% greater than the diameter of the contralateral transverse sinus; the remaining patients were in group B. Quantitative DSA was used to calculate cerebral circulation time. Cerebral circulation time was defined as the time difference between the relative time to maximal intensity of ROIs in the proximal internal carotid artery and the internal jugular vein. ΔCCT was defined as cerebral circulation time before stent placement minus cerebral circulation time after stent placement. ΔCCT, white matter hyperintensity signals, and sulcal effacement in MR imaging were compared between the 2 groups. ΔCCT was significantly shorter in group A (0.65 ± 1.3) than in group B (-0.12 ± 1.4). Three patients had white matter hyperintensity signals in group A, and 1 developed hyperperfusion syndrome. Group B showed no MR imaging signs of hyperperfusion syndrome. Ipsilateral hypoplastic transverse sinus was associated with prolonged cerebral circulation time before stent placement and greatly shortened cerebral circulation time after stent placement. Inadequate venous drainage might play a role in impaired cerebral autoregulation and might influence the development of poststenting hyperperfusion syndrome.

Quantitative cerebral perfusion assessment using microscope-integrated analysis of intraoperative indocyanine green fluorescence angiography versus positron emission tomography in superficial temporal artery to middle cerebral artery anastomosis.

Background:Intraoperative qualitative indocyanine green (ICG) angiography has been used in cerebrovascular surgery. Hyperperfusion may lead to neurological complications after superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis. The purpose of this study is to quantitatively evaluate intraoperative cerebral perfusion using microscope-integrated dynamic ICG fluorescence analysis, and to assess whether this value predicts hyperperfusion syndrome (HPS) after STA-MCA anastomosis.Methods:Ten patients undergoing STA-MCA anastomosis due to unilateral major cerebral artery occlusive disease were included. Ten patients with normal cerebral perfusion served as controls. The ICG transit curve from six regions of interest (ROIs) on the cortex, corresponding to ROIs on positron emission tomography (PET) study, was recorded. Maximum intensity (IMAX), cerebral blood flow index (CBFi), rise time (RT), and time to peak (TTP) were evaluated.Results:RT/TTP, but not IMAX or CBFi, could differentiate between control and study subjects. RT/TTP correlated (|r| = 0.534-0.807; P < 0.01) with mean transit time (MTT)/MTT ratio in the ipsilateral to contralateral hemisphere by PET study. Bland–Altman analysis showed a wide limit of agreement between RT and MTT and between TTP and MTT. The ratio of RT before and after bypass procedures was significantly lower in patients with postoperative HPS than in patients without postoperative HPS (0.60 ± 0.032 and 0.80 ± 0.056, respectively; P = 0.017). The ratio of TTP was also significantly lower in patients with postoperative HPS than in patients without postoperative HPS (0.64 ± 0.081 and 0.85 ± 0.095, respectively; P = 0.017).Conclusions:Time-dependent intraoperative parameters from the ICG transit curve provide quantitative information regarding cerebral circulation time with quality and utility comparable to information obtained by PET. These parameters may help predict the occurrence of postoperative HPS.

Angiographic Circulation Time and Cerebral Blood Flow during Balloon Test Occlusion of the Internal Carotid Artery

Angiography-based balloon test occlusion (BTO) has been empirically used to predict tolerance to permanent carotid artery occlusion. We tested the hypothesis that the laterality of the hemispheric circulation time (HCT) of the contrast medium at cerebral angiography would reflect bilateral asymmetry of the cerebral blood flow (CBF) during BTO. Thirty-one consecutive patients who underwent BTO of the internal carotid artery were retrospectively analyzed. HCT was defined as the interval between the time-to-peak in the middle cerebral artery and the cortical veins calculated using time-density curve. The difference in HCT between the occluded and nonoccluded side was calculated at the carotid or dominant vertebral angiograms obtained during BTO. We estimated the correlation between the difference in HCT and bilateral asymmetry of the CBF, which was quantitatively determined by single-photon emission computed tomography. The HCT was 5.3±1.5 seconds and regional CBF was 41.3±11.3 mL/100 g per minute in the occluded side, compared with 3.6±0.9 seconds and 48.4±14.9 mL/100 g per minute in the nonoccluded side, respectively. The difference in HCT was strongly correlated with the asymmetry ratio of the CBF (r(2)=0.89, P<0.0001). Angiographically based measurement of the cerebral circulation time can provide valuable information concerning cerebral hemodynamics.

Multiple Sclerosis: Cerebral Circulation Time

To assess cerebral circulation times (CCTs) in patients with multiple sclerosis (MS) and control subjects by using contrast material-enhanced ultrasonography (US) to determine whether vascular abnormalities can be detected in this disease. This study was approved by the local ethics committee, and informed consent was obtained from all subjects. One hundred three patients with MS and 42 control subjects underwent extracranial and transcranial venous echo-color Doppler ultrasonography (US) and contrast-enhanced US. CCT was defined as the difference in arrival time of the US contrast agent bolus between the carotid artery and the internal jugular vein. The presence of chronic cerebrospinal venous insufficiency (CCSVI) was defined according to previously reported criteria for the extracranial and transcranial US techniques. Nonparametric statistics, including the Mann-Whitney U test and the Kruskal-Wallis analysis of variance, were used to compare contrast-enhanced US parameters between groups. The longest and average CCTs were substantially prolonged in patients with MS compared with those in control subjects (median longest CCT in patients with MS, 6.47 seconds [range, 3.29-29.24 seconds]; that in control subjects, 5.54 seconds [range, 2.57-7.63 seconds]; P < .001; median average CCT in patients with MS, 5.76 seconds [range, 2.64-17.51 seconds]; that in control subjects, 5.01 seconds [range, 2.57-7.06 seconds]; P < .002). No correlation was found between CCTs and clinical parameters. The prevalence of CCSVI was higher in patients with MS than in control subjects (77% vs 28%, P < .0001). CCT was not significantly different between patients with MS who had CCSVI and patients with MS who did not (P = .182). These results suggest that contrast-enhanced US with CCT assessment may have a role in the evaluation of cerebral blood flow in patients with MS and that a vascular impairment could be associated with MS. The finding of a prolonged CCT at contrast-enhanced US does not result from outflow impairment. Further studies are required to verify these observations and to clarify if CCT and CCSVI have any physiologic and clinical relevance in MS.

Intraprocedural Prediction of Hemorrhagic Cerebral Hyperperfusion Syndrome After Carotid Artery Stenting

Hyperperfusion syndrome (HPS) is a rare but severe complication after carotid artery stenting (CAS). Reliable methods for predicting HPS remain to be developed. We aimed to establish a predictive value of hemorrhagic HPS after CAS. Our retrospective study included 136 consecutive patients who had undergone CAS. We determined the cerebral circulation time (CCT) by measuring the interval between the point of maximal opacification of the terminal portion of the internal carotid artery and the cortical vein. We calculated intraprocedural CCT changes (ΔCCT) by subtracting postprocedural CCT values from preprocedural CCT values. The mean ΔCCT was 0.9 ± 0.9 seconds; 3 patients (2.2%) with prolonged ΔCCT (2.7, 5.4, and 5.8 seconds) developed HPS. The cutoff time of 2.7 seconds predicted hemorrhagic HPS retrospectively with 100% sensitivity and 99% specificity. Our findings suggest that post-CAS HPS can be predicted by using the ΔCCT value obtained by intraprocedural digital subtraction angiography. Patients with a ΔCCT >2.7 seconds require careful intensive hemodynamic and neurologic monitoring after CAS.

Measurement of cerebral circulation times using dynamic whole-brain CT-angiography: feasibility and initial experience

The objective of the study was to use 320-detector row 4D CT angiography (CTA) for measuring cerebral circulation times (CCT) and to assess early venous drainage (EVD) and shortening of CCT in arteriovenous malformations (AVM) and to compare with DSA. CCT of 12 physiological patients and five AVM patients were acquired using a 4D CTA protocol by recording cerebrovascular bolus passage time. In the AVM patients EVD time (EVDT) was measured. Identical measurements were performed on DSA for the AVM patients. It was found that the physiological CCTs were 5.8 ± 1.4 s (M ± SD). EVD was seen in all AVMs and resulted in a shortened CCT of 3.4 ± 1.1 s (p = 0.01). There was no significant difference for CCT and EVDT values derived from DSA and 4D CTA. Thus, the CCTs can be measured non-invasively using clinical 4D CTA. Early venous drainage with shortened CCTs was observed by 4D CTA in all five patients with AVMs.

Procedural predictors of delayed cerebral infarction after intra-arterial vasodilator infusion for vasospasm following aneurysmal subarachnoid hemorrhage

The goals of this study were to identify predictors of delayed cerebral infarction in aneurysmal SAH after intra-arterial (IA) vasodilator infusion and to select proper parameters for treatment success. Forty-three patients qualified for review. Cerebral infarction was determined by DWI within 1 week of angiographic vasospasm. Infarction developed in 18 of the 43 patients (41.9%) after IA vasodilator infusion and was associated with a high degree of proximal vessel residual narrowing and angiographic cerebral circulation time (CCT) prolongation at the end of IA vasodilator infusion (p < 0.001). A high degree of proximal residual narrowing (p = 0.018; odds ratio = 1.071; 95% confidence interval [CI] 1.012-1.123) and CCT prolongation at the end of the procedure (p = 0.007; odds ratio = 2.203; 95% CI 1.254-4.232) were found to be predictors of infarction by multivariate analysis. Furthermore, receiver operating characteristic (ROC) curves showed that both variables predicted the development of infarction (proximal vessel residual narrowing, area under the ROC curve [AUC], 0.828; CCT, AUC, 0.866). When proximal vessel narrowing of >30% or a CCT of >7 s by final angiography during IA vasodilator infusion were used as a threshold, the negative predictive value for infarction was 88.9% (95% CI 65.3-98.6%), and when narrowing was >30% and CCT was >7 s, the probability of subsequent cerebral infarction was 100% (95% CI 71.7-100%). Angiographic CCT and residual narrowing at the end of IA vasodilator infusion were found to predict the subsequent occurrence of cerebral infarction. The authors suggest that residual narrowing of 30% and a CCT of 7 s could be used as a minimum indicator of IA vasodilator infusion endpoints.

Intraprocedural Changes in Angiographic Cerebral Circulation Time Predict Cerebral Blood Flow After Carotid Artery Stenting

Changes in the cerebral blood flow (CBF) are important for planning postoperative care in patients treated by carotid artery stenting (CAS). The relationship between intraprocedural changes in the angiographic cerebral circulation time (CCT) and perioperative CBF changes were retrospectively studied in 49 CAS procedures performed in 46 patients with carotid artery stenosis. The CCT, defined as the interval between the timing of maximal opacification at the terminal portion of the internal carotid artery and at the cortical vein, was determined by referring to time-density curves of data obtained from routine intraprocedural digital subtraction angiography. The intraoperative change in CCT (Delta CCT) was calculated for each of the 49 procedures. CBF studies, using dynamic perfusion computed tomography, were performed 10-2 days before and 2-4 days after CAS. Perioperative changes in the ratio of the CBF in the territory of the middle cerebral artery on the affected side to CBF on the contralateral side (%CBF) were calculated by subtracting pre- from postoperative %CBF (Delta%CBF) and the correlation between Delta CCT and Delta%CBF was evaluated. Mean CCT was shortened by 1.1 seconds from 5.3 to 4.2 seconds after CAS. Mean %CBF increased by 11.9% from 91.8% to 103.7% after the procedure. Delta CCT and Delta%CBF showed a significant positive correlation (r = 0.61, p = 0.008). Intraprocedural changes in angiographic CCT are predictive of postoperative CBF in patients with CAS.

Intra-arterial colforsin daropate for the treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Cerebral vasospasm (CV) remains a major cause of mortality and morbidity in patients with subarachnoid hemorrhage (SAH). Here, we examined the effectiveness and safety of intra-arterial injection of colforsin daropate hydrochloride (CDH). A consecutive series of 29 patients with angiographically confirmed CV received intra-arterial CDH (IAC) therapy. Angiographic changes in spastic vessels and the cerebral circulation time (CCT) were assessed before and after IAC treatment, together with the change in clinical status. IAC treatment was performed in 53 procedures in 29 patients. Angiographic improvement was observed following all procedures (100%), and clinical improvement was observed following 36 of 42 procedures (86%) in symptomatic cases. CCT improved significantly. At the 3-month follow-up, 19 patients (66%) showed good recovery or moderate disability on the Glasgow Outcome Scale. Major adverse effects were headache and increased heart rate. IAC treatment was effective and safe for the treatment of CV after SAH.

Serial measurements of quantitative EEG and cerebral blood flow and circulation time after brain infarction.

The quantitative EEG (QEEG), regional cerebral blood flow (rCBF) and circulation time of 17 patients were examined semisimultaneously thrice during the first 3 months after a cerebral supratentorial infarction. The EEG was quantified according to normalized slope descriptor technique in nine patients and by means of a combined period and amplitude analysis in eight patients. Intravenously injected isotopes 133Xenon and 99TcmO4 were used for blood flow and circulation time measurements. The QEEG-values improved during the whole follow-up period. Cerebral blood flow stayed low for all 3 months and did not alter during this period, while initially prolonged circulation time to some extent improved within 2 weeks remaining, however, prolonged even thereafter. A tendency for a positive correlation between QEEG and rCBF values in the infarcted hemisphere could be seen.

Estimating the Volume of Cerebral Aneurysms: Method Error versus Volume Variation over Time

To the Editor: The theoretical volumetric filling of a cerebral aneurysm after endovascular coiling (“packing density”) has been considered an indicator of long-term aneurysm occlusion. The volumetric filling is the volume of all coils implanted expressed as a percentage of the aneurysm volume. While the volumes of the coils are easily and precisely calculated using the cylindrical volume equation (assigning outer coil diameters and lengths according to product specification), the method error in estimating aneurysm volume has been a matter of concern. The recent article by Hanley et Al.1 brings another contribution to this question. In this study, the volumes of silicone models of cerebral aneurysms were accurately measured, and compared to volume estimates obtained by DSA, CTA and MRA as interpreted by four independent observers. Their results indicated error rates of 14% to 19% in aneurysm volume calculations regardless of imaging modality. These results are not unexpected. Substantial differences in aneurysm volume estimation can result from adding or subtracting a few pixels in caliper measurements, it is almost impossible to obtain the same volume estimate on repeated manual imaging segmentation and threshold settings of 3D reconstructions, and systematic differences should not be surprising when using different image acquisition modalities. I write to point out a major difficulty in doing accurate and repeatable measurements of aneurysm volume that has not been given appropriate attention, that is, that aneurysm volume can change considerably over the heart cycle. Studies with cine phase-contrast MRA2, and with transcranial power Doppler ultrasound3,4, showed that intracranial saccular aneurysms undergo changes in size during the cardiac cycle, expanding in systole and contracting in diastole. In the MRA study2 pulsatile volume changes were seen to be larger in ruptured aneurysms (51% on average, ranging in individual cases from 38% to 68%) than in unruptured aneurysms (17.6% in average, ranging from 0% to 33%). For the same aneur­ysm the expansibility is larger at higher levels of intracranial pressure4, and after a decrease in intracranial pressure (after insertion of ventricular draina­ge in patients with hydroce­phalus after subarachnoid hemorrhage) the aneurysm volume becomes less unstable from systole to diastole, but the aneurysm increases in size4. Dynamic aneurysm volume changes probably explain the fact that the coil mesh can be larger than the measured aneurysm size before coiling5. These dynamic changes in aneur­ysm size are usually not observable on DSA because this technique does not obtain rapid images through the cardiac cycle, but in my experience (which is probably also the reader’s), visible pulsatile changes in aneurysm volume can be observed in some instances on source images of rotational 3D angiography, especially in ruptured aneurysms (however, the volume change in such conditions is difficult to quantify since the images in systole and diastole are taken in different projections during the rotational run). However, there is at least one published report of huge volume increase of an aneurysm from diastole to systole (230%) on DSA images in a patient with an anterior communicating aneurysm, when the cerebral circulation time was prolonged because of severe intracranial hypertension6. Hanley et Al1 also noted a modality-specific error in measuring aneurysm volume in their model of known and stable aneurysm volume: CTA tended to overestimate and MRA tended to underestimate aneurysm volume, while larger scatter was the case for DSA. The modality-specific error is probably not the same in this study as in real aneurysms, since different imaging modalities should also be affected by different aspects of the dynamics of aneurysm volume. In conclusion, estimates of aneurysm volume probably cannot be done with the high level of accuracy that has been looked for. Thus, one should be less dogmatic in searching for safety thresholds of packing density. When the immediate result of an operation is a well-filled aneurysm with a visually dense coil mesh, there is no angiographic opacification of the aneur­ysm or only a small neck remnant, and the operator cannot safely do more, it is probably not relevant whether the estimate of packing density is imprecise by, say, more or less one fifth of the estimate. Nevertheless, I think that the packing density is to be carefully calculated after each case using the available estimate of aneurysm volume, and the value is to be annotated in the operation file as a routine procedure, because it is intuitively a quality indicator of the procedure (a high packing density is surely better than a low one).

ADMISSION ANGIOGRAPHIC CEREBRAL CIRCULATION TIME MAY PREDICT SUBSEQUENT ANGIOGRAPHIC VASOSPASM AFTER ANEURYSMAL SUBARACHNOID HEMORRHAGE

Angiographic cerebral vasospasm occurs in approximately 70% of patients hospitalized after aneurysmal subarachnoid hemorrhage (SAH) and is associated with poor outcome. In this study, we examined whether or not cerebral circulation time (CCT) measured with digital subtraction angiography was associated with angiographic vasospasm. Patients who underwent cerebral angiography within 24 hours of SAH were analyzed. Contrast dye transit time from the arterial to the venous phase was measured to obtain CCT (supraclinoid internal carotid artery to parietal cortical veins) and microvascular CCT (cortical middle cerebral artery to parietal cortical veins). Patients with ruptured anterior circulation aneurysms and vasospasm on follow-up angiography (Group A) were compared with patients with SAH without vasospasm (Group B) and with normal control subjects (Group C). There were 20 patients in Group A (mean age, 51 +/- 13 yr), 17 patients in Group B (56 +/- 12 yr), and 98 patients in Group C (52 +/- 12 yr). CCT in patients in Group A (7.7 +/- 1.9 s) was significantly longer than those in Groups B (6.6 +/- 1.2 s; P = 0.005) and C (5.9 +/- 1 s; P < 0.001). Microvascular CCT in patients in Group A (7.1 +/- 1.8 s) was significantly longer than those in Groups B (6.1 +/- 1.2 s; P = 0.003) and C (5.4 +/- 0.9 s; P < 0.001). Prolonged CCT, a measurement of increased small vessel resistance, can be identified within 24 hours after SAH and is associated with subsequent angiographic vasospasm. These results suggest that microcirculation changes may be involved in vasospasm.

Impairment of Cerebral Perfusion and Infarct Patterns Attributable to Vasospasm After Aneurysmal Subarachnoid Hemorrhage

The objective of this study was to investigate disturbance of perfusion and infarct patterns attributable to cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). One hundred seventeen patients with aneurysmal SAH specifically selected at high risk for CVS were enrolled in this prospective study. One hundred twelve patients underwent surgical (n=63) or endovascular (n=59) therapy. For assessment of CVS, relative diameter changes of proximal and distal vessel segments on follow-up angiography at day 7+/-3 after SAH were analyzed in relation to baseline measurements, and cerebral circulation times were measured. Postprocedure MRI was undertaken selectively at four time points: within 3 days, between days 4 and 6, day 7 to 14, and day 15 to 28 from onset of SAH, including perfusion- and diffusion-weighted images. Procedure-related lesions were excluded and CVS-associated infarct patterns analyzed. Occurrence of angiographic CVS was as high as 87.5% between days 7 and 14 and 52.5% showed new infarcts. Eighty-one percent of the infarcts were related to severe CVS (vascular narrowing >66%) and significant (P<0.001) cerebral circulation times prolongation of 8.47+/-2.25 seconds (time-to-peak delay on perfusion-weighted image: 6.52+/-4.75 seconds), 16% were associated with moderate CVS (34% to 66% vascular narrowing; cerebral circulation times prolongation: 4.72+/-0.66 seconds). Besides territorial (47%), lacunar (20%), and watershed infarcts (26%), in 7%, band-like cortical lesions developed without evidence for severe CVS. CVS after SAH may involve the complete arterial system from the circle of Willis up to the distal vessel segments. Depending on the variable types of collateral flow, location of affected vessels segments as well as the degree of CVS may induce different infarct patterns.

Transcranial and extracranial ultrasound assessment of cerebral hemodynamics in vascular and Alzheimer's dementia

Background: Increasing life expectancy of the population leads to a higher incidence of dementia. Exact differentiation between the most common types, vascular dementia (VD) and Alzheimer's dementia (AD), is crucial to the development and application of new treatment strategies. Both conditions are thought to differ greatly by their extent of microvascular affection. Transcranial and extracranial ultrasound permits analysis of cerebral hemodynamics and should help to differentiate between VD and AD. We compare multimodal ultrasound data between VD, AD and controls, and give an overview of the literature on this topic.Methods: Twenty VD and 20 AD patients were studied and compared with 12 age-matched controls. Transcranial color-coded ultrasound was performed to assess blood flow velocity (Vmean) and pulsatility indices (PI) of the middle cerebral artery (MCA). Extracranial duplex and Doppler ultrasound techniques were used to assess the blood volume flow (BVF) in the anterior circulation (both internal carotid arteries [ICA]) and posterior circulation (both vertebral arteries [VA]), the global cerebral blood flow (CBF = BVFICA + BVFVA), the global cerebral circulation time (CCT = time delay of echo–contrast bolus arrival between ICA and internal jugular vein) and global cerebral blood volume (CBV = CCT × CBF).Results: MCA Vmean in VD (36 ± 8 cm/s) and AD (43 ± 13 cm/s) were significantly lower than in controls (59 ± 13 cm/s) but did not differ significantly between VD and AD groups. PI (1.1 ± 0.2; 1 ± 0.2; 0.9 ± 0.2) only differed significantly between VD group and controls. CBF and CCT in VD (570 ± 61 ml/min; 8.8 ± 2.6 s) and AD (578 ± 77 ml/min; 8.2 ± 1.4 s) were similar but differed significantly from controls (733 ± 54 ml/min; 6.4 ± 0.8 s). BVF in the anterior and posterior circulation of VD group (412 ± 62 and 158 ± 38 ml/min) and AD group (428 ± 62 and 150 ± 41 ml/min) were significantly lower than in controls (537 ± 48 and 199 ± 26 ml/min) but did not differ significantly between the patient groups.Discussion: Transcranial and extracranial ultrasound does not help to distinguish between VD and AD. However, our results add insight into the pathophysiology of dementia, arguing in favor of a common 'vascular' pathway in both conditions.

Ultrasonographic measurement of cerebral blood flow, cerebral circulation time and cerebral blood volume in vascular and Alzheimer’s dementia

Vascular dementia (VD) and Alzheimer's dementia (AD) are the most common differential diagnoses in patients with cognitive impairment. Although of different etiology, small vessel disease is postulated to be present in both conditions. We investigated global cerebral blood flow (CBF), global cerebral circulation time (CCT) and global cerebral blood volume (CBV) in VD and AD patients using a multimodal ultrasound (US) approach. 20 VD and 20 AD patients were included and compared with 12 age-matched controls. Duplex US of both internal carotid and vertebral arteries was performed to measure CBF. CCT was defined as the time delay of an echo-contrast bolus arrival between the internal carotid artery and internal jugular vein using extracranial Doppler. CBV was calculated as the product of CBF and CCT. CBF was significantly lower (VD: 570 +/- 61; AD: 578 +/- 77; controls: 733 +/- 54 ml/min) and CCT significantly longer (8.8 +/- 2.6; 8.2 +/- 1.4; 6.4 +/- 0.8 s) in both patient groups compared with controls (p < 0.003). No difference in CBF and CCT was found between the two patient groups. CBV was similar in all three groups (82 +/- 20; 79 +/- 19; 78 +/- 9 ml). The equally reduced CBF and prolonged CCT in VD and AD support the hypothesis, that small vessel disease is a relevant factor in both types of dementia. The presented multimodal US approach helps to assess the extent of changes in the global cerebral hemodynamics in patients with dementia but does not allow a differentiation between VD and AD.

Assessment of changes in cerebral circulation time due to vasospasm in a specific arterial territory: effect of angioplasty

This study demonstrates that in experienced hands, intracranial angioplasty is a feasible and safe option in a selected group of patients with severe (>50% stenosis) symptomatic vasospasm following subarachnoid hemorrhage. Cerebral circulation time is a surrogate parameter closely linked to cerebral perfusion. The study presented shows that not only stenosis but also changes in circulation time are obtained by angioplasty. Twenty angioplasties of one or two vessel segments were performed over 2 years in 18 consecutive patients with posthemorrhagic vasospasm fulfilling criteria for invasive treatment. In all patients, degree of stenosis and circulation time could be reduced by angioplasty. Clinical results were ranked according to Glasgow Outcome Scale. Imaging after 15/20 angioplasties showed no additional infarction. In 4/20 cases, CT showed demarcation of infarction after angioplasty. In 1/20 cases of posterior circulation angioplasty, CT is not sensitive enough to exclude smaller infarctions. Imaging and clinical outcome reveal a definite benefit.

Intra-Arterial Papaverine Infusions for the Treatment of Cerebral Vasospasm Induced by Aneurysmal Subarachnoid Hemorrhage

Cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage that has become refractory to maximal medical management can be treated with selective intra-arterial papaverine infusions. Papaverine is a potent vasodilator of the proximal, intermediate, and distal cerebral arteries and can improve cerebral blood flow (CBF). When infused intra-arterially using endovascular microcatheter techniques, papaverine can effectively increase angiographic vessel diameter, decrease prolonged cerebral circulation time, and improve cerebral oxygenation. However, one of the major disadvantages of papaverine is its transient nature, which can result in recurrent and/or persistent angiographic and clinical vasospasm that may require multiple repeated infusions, despite a successful response to the initial treatment. Intra-arterial papaverine can be used alone or in combination with balloon angioplasty. This article reviews the mechanism of action, technique of administration, effects on CBF, clinical results, and complications of intra-arterial papaverine for the treatment of cerebral vasospasm.

Angiographic assessment of cerebral circulation time for outcome prediction in patients with subarachnoid hemorrhage

Background In the acute stage following subarachnoid hemorrhage (SAH), prolonged cerebral circulation time reflects increased intracranial pressure (ICP), which can lead to irreversible brain damage. We evaluated the ability of cerebral circulation time to predict outcome in SAH patients. Methods We prospectively studied 40 consecutive patients treated for SAH according to standard intensive care guidelines. Lateral views in preoperative carotid digital subtraction arteriograms (DSA) were used to determine arteriovenous transit time (AVTT), defined as interval from initial opacification of the intracranial internal carotid artery to that of the Rolandic vein. We then analyzed relationship of AVTT to other prognostic parameters and outcome. Results AVTT depended on initial Glasgow Coma Scale score (GCS), ranging from 3.4 to 8.0 seconds (mean: 5.4) when initial GCS was 13 to 15; from 4.5 to 8.7 seconds (mean: 6.4) when initial GCS was 7 to 12; and from 5.8 to 15.0 seconds (mean: 9.1 seconds, excluding angiograms with nonfilling) when initial GCS was 3 to 6. AVTT correlated significantly with prognosis, longer AVTT predicting poorer outcome. No patient with an AVTT above 12 seconds recovered to a functioning state. Conclusions AVTT obtained from routinely performed acute-phase DSA in SAH patients reflects ICP and functional prognosis, representing a cost-effective, practical, and reliable outcome predictor.

Ultrasonographic assessment of global cerebral blood volume in healthy adults.

The authors describe a new ultrasonographic method for analysis of global cerebral blood volume (CBV) and its application under controlled hyperventilation. CBV was determined as the product of global cerebral blood flow volume (CBF) and global cerebral circulation time. CBF was measured by duplex sonography and calculated as the sum of flow volumes in both internal carotid arteries and vertebral arteries. Extracranial Doppler assessed cerebral circulation time by determining the time interval of echo-contrast bolus arrival between internal carotid artery and contralateral internal jugular vein. Forty-four healthy volunteers (mean age 45 +/- 19 years, range 20-79 years) were studied. Mean CBV was 77 +/- 13 mL. CBV did not correlate with age, end-tidal carbon dioxide level, heart rate, or blood pressure. Hypocapnia was induced in 10 subjects by controlled hyperventilation. Mean reduction of end-tidal carbon dioxide values by 9 +/- 1 mm Hg led to a significant increase in cerebral circulation time (6.1 +/- 0.9 to 8.4 +/- 1.1 second, P < 0.0001) and a significant CBF decrease (742 +/- 85 to 526 +/- 77 mL/min, P < 0.0001), whereas CBV remained unchanged (75 +/- 6 to 73 +/- 10 mL).

Microcirculatory changes during acute phase of aneurysmal sub-arachnoid hemorrhage evaluated by clinical and experimental studies

Cerebral microcirculatory changes during cerebral vasospasm after aneurysmal sub-arachnoid hemorrhage (SAH) are still controversial and uncertain. Experimental and clinical investigations of cerebral microcirculation after SAH were performed.Experimental SAH was produced by a canine two-hemorrhage method, and the dogs were perfusion-fixed at 3, 7 and 14 days after SAH. Specimens of the anterior sylvian gyri and pons were produced by three methods. Microvascular corrosion casts produced by arterial injection of polyester resin were examined by scanning electron microscopy (SEM). Sectioned slices parallel to the brain surface were examined by SEM and by light microscopy with morphometric analysis of the luminal diameter and wall thickness of the small arteries. Corrosion casts showed tapered narrowing in the arterioles and irregular width with folds in the perforating arteries 3 to 7 days after SAH. Sectioned slices showed increased wall thickness and decreased internal diameter of the arterioles and the perforating arteries 3 to 7 days after SAH.In cases with aneurysmal SAH, regional cerebral blood flow (rCBF) and digital subtraction angiography (DSA) were performed. Also, cerebral circulation time (CCT) obtained by analyzing the time–density curve of the contrast media on DSA images was evaluated in association with rCBF and angiographic vasospasm. In addition to correlation between the degree of angiographic vasospasm and rCBF, CCT showed strong inverse correlation with rCBF, and even in mild angiographic vasospasm, prolonged peripheral CCT was clearly associated with decreased rCBF.These results suggest that intraparenchymal small arteries decrease their caliber, which results in increased small-vessel resistance and affects cerebral ischemia during cerebral vasospasm.