Abnormal Cranial Magnetic Resonance Imaging Scans in Sickle-cell Disease

Kugler, Steven L.; Anderson, Brenda J.; Cross, Dewitt; Sharif, Zafar; Sano, Mary; Haggerty, Rita; Prohovnik, Isak; Hurlet‐Jensen, Anne; Hilal, S. K.; Mohr, J. P.; Vivo, Darryl C. De

doi:10.1001/archneur.1993.00540060059019

Cited by 79 publications

(47 citation statements)

References 28 publications

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“…14,15 However, this effect will not be very prominent, because the infarcts detected in this study were smaller than 5 mm in most patients.…”

Section: Discussionmentioning

confidence: 70%

“…19 The CBF measured in the present study is relatively low in comparison to previous studies that measured cerebral blood flow in patients with SCD using different techniques, reporting CBF varying from 65 to 153 mL/100 g/min. 11,14,15,19,27 Variation in measured CBF may be caused by differences in perfusion imaging techniques. Because estimation of CBF is not standardized to an absolute measure, values obtained by different techniques cannot be compared.…”

Section: Discussionmentioning

confidence: 99%

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Cerebral Blood Flow Measurement in Children With Sickle Cell Disease Using Continuous Arterial Spin Labeling at 3.0-Tesla MRI

Tweel¹,

Nederveen²,

Majoie³

et al. 2009

Stroke

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Background and Purpose-Cerebral infarction is an important complication of sickle cell disease (SCD) and occurs in one third of the patients with SCD. The risk of infarction is commonly attributed to the hyperemia that is associated with anemia and reduces the cerebral vascular reserve. We measured regional cerebral blood flow (rCBF) by continuous arterial spin labeling MRI, which is a noninvasive method that does not require ionizing radiation. The purpose of this study was to examine rCBF in children with SCD and compare it with rCBF in healthy children. Methods-rCBF was measured at 3-T continuous arterial spin labeling MRI in 24 neurological normal patients with SCD and in 12 healthy children matched for ethnicity and age (mean age in both groups 13 years). rCBF was calculated for 6 vascular territories (left and right anterior, middle and posterior cerebral artery). Asymmetry in rCBF was evaluated by measuring differences in flow between left and right hemispheres. The definition of asymmetry (Ͼ11.7 mL/100 g/min) was based on a repeatability study performed in 6 healthy adults. Results-The rCBF was of similar magnitude in patients with SCD and control subjects in the frontal, middle, and posterior territories. The majority of patients with SCD (58%) demonstrated a left-right asymmetry of rCBF in one or more vascular territories, whereas none of the control subjects did. Conclusion-In contrast to previous studies, we found no difference in cerebral blood flow between patients and control subjects. We did observe an asymmetry in rCBF in the majority of patients with SCD that was not present in healthy control subjects. (Stroke. 2009;40:795-800.)

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“…14,15 However, this effect will not be very prominent, because the infarcts detected in this study were smaller than 5 mm in most patients.…”

Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Cerebral Blood Flow Measurement in Children With Sickle Cell Disease Using Continuous Arterial Spin Labeling at 3.0-Tesla MRI

Tweel¹,

Nederveen²,

Majoie³

et al. 2009

Stroke

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“…[5][6][7] Because children with HbSS who have had one stroke are known to be at high risk for subsequent events, [8][9][10] there has been concern that children with silent lesions also may be at increased risk for recurrence. 11 Should that be the case, subsequent lesions might occur in a location and be of sufficient size to cause neurologic deficits, fulfilling the usual definition for stroke.…”

Section: Introductionmentioning

confidence: 99%

Longitudinal changes in brain magnetic resonance imaging findings in children with sickle cell disease

Pegelow

2002

Blood

312

260

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Children with sickle cell anemia (HbSS) are at high risk for neurologically overt cerebral infarcts associated with stroke and neurologically silent cerebral infarcts correlated with neuropsychometric deficit. We used complete magnetic resonance imaging (MRI) histories from 266 HbSS children, aged 6 through 19 years, who were enrolled in the Cooperative Study of Sickle Cell Disease (CSSCD) to examine silent infarct prevalence, localization, recurrence, and progression. We report a baseline prevalence of 21.8%, marginally higher than previously reported due to improved imaging technologies. Although we observed no overall sex difference in prevalence, most lesions in girls occurred before age 6, whereas boys remained at risk until age 10. Silent infarcts were significantly smaller and less likely to be found in the frontal or parietal cortex than were infarcts associated with stroke. Children with silent infarct had an increased incidence of new stroke (1.03/100 patientyears) and new or more extensive silent infarct (7.06/100 patient-years) relative to stroke incidence among all children in our cohort (0.54/100 patient-years). Both events were substantially less frequent than the risk of stroke recurrence among children not provided chronic transfusion therapy. Although chronic transfusion is known to decrease occurrence of new silent infarcts and strokes in children with elevated cerebral arterial blood flow velocity, further study is required to determine its risk-benefit ratio in children with silent infarct and normal velocities. Until safe and effective preventive strategies against infarct recurrence are discovered, MRI studies are best reserved for children with neurologic symptoms, neuropsychometric deficits, or elevated cerebral artery velocities. (Blood. 2002;99: 3014-3018)

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“…These patients with silent lesions predispose to the development of new or progressive neurological silent lesions (Wang et al 1998). Furthermore, among the various clinical and laboratory parameters, the presence of silent infarctions on MRI was the strongest independent risk factor for stroke and was associated with a 14 fold increased risk factor of developing overt stroke (Kugler et al 1993;Pegelow et al 2002;Hoppe 2005). Kral et al (2003) have reported that the frontal lobes of the brain were most vulnerable to cerebro-vascular injury in SCD patients.…”

Section: Discussionmentioning

confidence: 99%