Inverse correlation between cerebral blood flow measured by continuous arterial spin-labeling (CASL) MRI and neurocognitive function in children with sickle cell anemia (SCA)

Strouse, John J.; Cox, Christiane; Melhem, Elias R.; Lu, Hanzhang; Kraut, Michael A.; Razumovsky, Alexander Y.; Yohay, Kaleb; Zijl, Peter C. van; Casella, James F.

doi:10.1182/blood-2005-10-4029

Cited by 77 publications

(107 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is in line with previously documented data on cerebral hyperemia in children with SCD that were obtained by ASL as well as other techniques such as the 133Xe inhalation method or positron emission tomography (PET) (10)(11)(12)(30)(31)(32). Also, mean flow and velocity assessed by PC-MRI were higher in patients than in controls, supporting the finding of hyperemia in children with SCD, which is likely to be anemia related (32).…”

Section: Discussionsupporting

confidence: 90%

“…Third, we found less and smaller perfusion asymmetries than in previous studies, in which continuous and pulsed ASL sequences were employed with 1200 to 1400 msec postlabeling delays (10)(11)(12)(13). In the current study, significant perfusion asymmetries were also encountered in controls using a short postlabeling delay.…”

Section: Discussionsupporting

confidence: 48%

“…All studies, however, identified CBF asymmetries that could be an early indicator of subclinical pathological changes in microvasculature or hemodynamics. The described perfusion asymmetries, however, could not always be associated with the presence of ischemic lesions (10)(11)(12)(13).…”

mentioning

confidence: 76%

See 2 more Smart Citations

Arterial spin labeling measurement of cerebral perfusion in children with sickle cell disease

Gevers

Nederveen

Fijnvandraat

et al. 2011

Magnetic Resonance Imaging

View full text Add to dashboard Cite

Purpose: To evaluate the applicability of arterial spin labeling (ASL) cerebral blood flow (CBF) measurements in children with sickle cell disease (SCD). Materials and Methods:We included 12 patients and five controls. Conventional magnetic resonance imaging (MRI) (T2, fluid attenuated inversion recovery [FLAIR], and MR angiography) was performed to diagnose silent infarcts, vasculopathy, or leukoencephalopathy. Pseudo-continuous ASL was performed to measure CBF using two postlabeling delays to identify transit-time effects. Perfusion estimates were corrected for hematocrit and blood velocity in the labeling plane and compared to phase-contrast MR. CBF asymmetries between the flow maps of the left and right internal carotid arteries were tested for significance using paired t-tests. Significant asymmetries were expressed in terms of an asymmetry ratio (AR ¼ absolute difference/mean). An AR >10% was considered clinically relevant.Results: Mean CBF was higher in patients than in controls. Agreement between CBF and flow improved after applying hematocrit and velocity corrections. At a 2100 msec postlabeling delay one patient had a clinically relevant asymmetry. No association was observed between CBF asymmetries and silent infarcts. Conclusion:Care must be taken in the interpretation of ASL-CBF measurements in SCD patients. A long postlabeling delay with blood velocity correction anticipates overestimation of CBF asymmetries.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 48%

See 1 more Smart Citation

Arterial spin labeling measurement of cerebral perfusion in children with sickle cell disease

Gevers

Nederveen

Fijnvandraat

et al. 2011

Magnetic Resonance Imaging

View full text Add to dashboard Cite

show abstract

“…Cerebral hyperemia in SCD has been amply documented previously, by several measurement methods (Brass et al, 1991;Oguz et al, 2003;Strouse et al, 2008), and is known to be anemia associated. We originally showed a linear relationship between normocapnic CBF and Hct (Prohovnik et al, 1989): within the nontransfused sample, the equation was fg = 231-3.88 Â Hct.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, Minniti et al (2004) suggested that transfusion normalized TCD velocities in patients with normal MRA, and thus, presumably reduced stroke risk by changing hemodynamics. Most recently, hyperemia has been confirmed in SCD patients in the absence of significant stenoses, as well as significant correlations between the level of hyperemia and cognitive deficits (Strouse et al, 2008).…”

Section: Stenosis Versus Hyperemia In Sickle-cell Diseasementioning

confidence: 93%

Hemodynamic Etiology of Elevated Flow Velocity and Stroke in Sickle-Cell Disease

Prohovnik

Hurlet‐Jensen

Adams

et al. 2009

J Cereb Blood Flow Metab

115

108

View full text Add to dashboard Cite

Elevation of blood flow velocity in the large cerebral vessels is known to be of substantial pathophysiologic and prognostic significance in sickle-cell disease (SCD). Its precise cause is not established, but the two obvious proximal mechanisms are obstructive vascular stenosis and hemodynamic dilatation. Here we revisit this distinction by analyzing cerebrovascular reserve capacity. Forty-two patients with SCD underwent measurements of global cerebral blood flow in grey matter by the 133 Xe inhalation method during normocapnia and hypercapnia to quantify cerebrovascular reactivity. Cerebral blood flow was significantly higher in SCD patients (120±31 ml/ 100 g/min) than in controls (76 ± 20 ml/100 g/min). Reactivity was significantly lower in SCD patients (1.06±1.92 versus 2.16±1.15%/mm Hg). Stepwise multiple regressions within the SCD sample determined that normocapnic cerebral blood flow was largely predicted by hematocrit (r = À0.59; P < 0.0001), whereas hypercapnic reactivity was only predicted by normocapnic flow across all subjects (r = À0.52; P < 0.0001). None of the controls, but 24% of the SCD patients showed 'steal' (negative reactivity, v 2 = 6.05; P < 0.02). This impairment of vasodilatory capacity, occurring at perfusion levels above 150 ml/100 g/min, may reflect intrinsic limitations of the human cerebrovascular system and can explain both the elevated blood flow velocities and the high risk of stroke observed in such patients.

show abstract

Hemorheological alterations, decreased cerebral microvascular oxygenation and cerebral vasomotion compensation in sickle cell patients

Waltz

Pichon

Mougenel³

et al. 2012

American J Hematol

View full text Add to dashboard Cite

Sickle cell anemia (SS) is characterized by a reduced cerebral microvascular oxygen saturation (cerebral TOI), which is not associated with hemoglobin concentration. Cerebral TOI has never been studied in sickle cell-hemoglobin C disease (SC). We focused on the relationships between hemorheological alterations and cerebral TOI in sickle cell patients with no cerebral vasculopathy and on the usefulness of TOI variability to assess the cerebral vasomotion activity. The blood rheological profile, the level of cerebral TOI (spatial resolved spectroscopy) and the cerebral TOI variability, which reflects vasomotion activity, were compared between 20 healthy subjects (AA), 21 SC patients, and 21 SS patients. Cerebral TOI exhibited the following order: AA > SC > SS. The low cerebral TOI in SS patients was related to red blood cell aggregation and deformability properties. The cerebral TOI variability of SS and SC patients was increased above healthy values and vasomotion activity was negatively associated with the reduced cerebral TOI in SS patients. We demonstrated that (1) blood rheology could be involved in the reduced cerebral TOI in SS patients but not in SC patients; (2) vasomotion activity is increased in SS and SC patients to compensate for the reduced cerebral TOI. Am. J. Hematol. 87:1070Hematol. 87: -1073Hematol. 87: , 2012

show abstract

Inverse correlation between cerebral blood flow measured by continuous arterial spin-labeling (CASL) MRI and neurocognitive function in children with sickle cell anemia (SCA)

Cited by 77 publications

References 18 publications

Arterial spin labeling measurement of cerebral perfusion in children with sickle cell disease

Arterial spin labeling measurement of cerebral perfusion in children with sickle cell disease

Hemodynamic Etiology of Elevated Flow Velocity and Stroke in Sickle-Cell Disease

Hemorheological alterations, decreased cerebral microvascular oxygenation and cerebral vasomotion compensation in sickle cell patients

Contact Info

Product

Resources

About