Differences in Activation and Deactivation in Children with Sickle Cell Disease Compared with Demographically Matched Controls

References

1. 1.↵
   2. Cohen MJ,
   3. Branch WB,
   4. McKie VC, et al

   . Neuropsychological impairment in children with sickle cell anemia and cerebrovascular accidents. Clin Pediatr (Phila) 1994;33:517–24 doi:10.1177/000992289403300902 pmid:8001319

   CrossRefPubMed
2. 2.↵
   2. Watkins KE,
   3. Hewes DK,
   4. Connelly A, et al

   . Cognitive deficits associated with frontal-lobe infarction in children with sickle cell disease. Dev Med Child Neurol 1998;40:536–43 pmid:9746006

   PubMedWeb of Science
3. 3.↵
   2. Wilimas J,
   3. Goff JR,
   4. Anderson HR Jr., et al

   . Efficacy of transfusion therapy for one to two years in patients with sickle cell disease and cerebrovascular accidents. J Pediatr 1980;96:205–08 doi:10.1016/S0022-3476(80)80803-1 pmid:7351580

   CrossRefPubMedWeb of Science
4. 4.↵
   2. Bernaudin F,
   3. Verlhac S,
   4. Freard F, et al

   . Multicenter prospective study of children with sickle cell disease: radiographic and psychometric correlation. J Child Neurol 2000;15:333–43 doi:10.1177/088307380001500510 pmid:10830200

   CrossRefPubMedWeb of Science
5. 5.↵
   2. Schatz J,
   3. Finke R,
   4. Roberts CW

   . Interactions of biomedical and environmental risk factors for cognitive development: a preliminary study of sickle cell disease. J Dev Behav Pediatr 2004;25:303–10 doi:10.1097/00004703-200410000-00001 pmid:15502546

   CrossRefPubMedWeb of Science
6. 6.↵
   2. Wang W,
   3. Enos L,
   4. Gallagher D, et al

   ; Cooperative Study of Sickle Cell Disease. Neuropsychologic performance in school-aged children with sickle cell disease: a report from the Cooperative Study of Sickle Cell Disease. J Pediatr 2001;139:391–97 doi:10.1067/mpd.2001.116935 pmid:11562619

   CrossRefPubMedWeb of Science
7. 7.↵
   2. Hijmans CT,
   3. Grootenhuis MA,
   4. Oosterlaan J, et al

   . Neurocognitive deficits in children with sickle cell disease are associated with the severity of anemia. Pediatr Blood Cancer 2011;57:297–302 doi:10.1002/pbc.22892 pmid:21671366

   CrossRefPubMedWeb of Science
8. 8.↵
   2. Steen RG,
   3. Emudianughe T,
   4. Hunte M, et al

   . Brain volume in pediatric patients with sickle cell disease: evidence of volumetric growth delay? AJNR Am J Neuroradiol 2005;26:455–62 pmid:15760849

   Abstract/FREE Full Text
9. 9.↵
   2. Steen RG,
   3. Langston JW,
   4. Ogg RJ, et al

   . Diffuse T1 reduction in gray matter of sickle cell disease patients: evidence of selective vulnerability to damage? Magn Reson Imaging 1999;17:503–15 doi:10.1016/S0730-725X(98)00204-5 pmid:10231177

   CrossRefPubMedWeb of Science
10. 10.↵
    2. Baldeweg T,
    3. Hogan AM,
    4. Saunders DE, et al

    . Detecting white matter injury in sickle cell disease using voxel-based morphometry. Ann Neurol 2006;59:662–72 doi:10.1002/ana.20790 pmid:16450382

    CrossRefPubMedWeb of Science
11. 11.↵
    2. Berkelhammer LD,
    3. Williamson AL,
    4. Sanford SD, et al

    . Neurocognitive sequelae of pediatric sickle cell disease: a review of the literature. Child Neuropsychol 2007;13:120–31 doi:10.1080/09297040600800956 pmid:17364569

    CrossRefPubMedWeb of Science
12. 12.↵
    2. Wang WC

    . Sickle-cell disease and compromised cognition. Pediatr Blood Cancer 2011;56:705–06 doi:10.1002/pbc.23000 pmid:21370400

    CrossRefPubMedWeb of Science
13. 13.↵
    2. Sun B,
    3. Brown RC,
    4. Hayes L, et al

    . White matter damage in asymptomatic patients with sickle cell anemia: screening with diffusion tensor imaging. AJNR Am J Neuroradiol 2012;33:2043–49 doi:10.3174/ajnr.A3135 pmid:22595904

    Abstract/FREE Full Text
14. 14.↵
    2. Smith SM,
    3. Fox PT,
    4. Miller KL, et al

    . Correspondence of the brain's functional architecture during activation and rest. Proc Natl Acad Sci U S A 2009;106:13040–45 doi:10.1073/pnas.0905267106 pmid:19620724

    Abstract/FREE Full Text
15. 15.↵
    2. Buckner RL,
    3. Andrews-Hanna JR,
    4. Schacter DL

    . The brain's default network: anatomy, function, and relevance to disease. Ann N Y Acad Sci 2008;1124:1–38 doi:10.1196/annals.1440.011 pmid:18400922

    CrossRefPubMedWeb of Science
16. 16.↵
    2. Zou P,
    3. Helton KJ,
    4. Smeltzer M, et al

    . Hemodynamic responses to visual stimulation in children with sickle cell anemia. Brain Imaging Behav 2011;5:295–306 doi:10.1007/s11682-011-9133-4 pmid:21881848

    CrossRefPubMedWeb of Science
17. 17.↵
    2. Darbari DS,
    3. Hampson JP,
    4. Ichesco E, et al

    . Frequency of hospitalizations for pain and association with altered brain network connectivity in sickle cell disease. J Pain 2015;16:1077–86 doi:10.1016/j.jpain.2015.07.005 pmid:26291276

    CrossRefPubMed
18. 18.↵
    2. Colombatti R,
    3. Lucchetta M,
    4. Montanaro M, et al

    . Cognition and the default mode network in children with sickle cell disease: a resting state functional MRI study. PLoS One 2016;11:e0157090 doi:10.1371/journal.pone.0157090 pmid:27281287

    CrossRefPubMed
19. 19.↵
    2. Salgado-Pineda P,
    3. Fakra E,
    4. Delaveau P, et al

    . Correlated structural and functional brain abnormalities in the default mode network in schizophrenia patients. Schizophr Res 2011;125:101–09 doi:10.1016/j.schres.2010.10.027 pmid:21095105

    CrossRefPubMed
20. 20.↵
    2. Laurienti PJ,
    3. Burdette JH,
    4. Wallace MT, et al

    . Deactivation of sensory-specific cortex by cross-modal stimuli. J Cogn Neurosci 2002;14:420–29 doi:10.1162/089892902317361930 pmid:11970801

    CrossRefPubMedWeb of Science
21. 21.↵
    2. Humphreys GF,
    3. Hoffman P,
    4. Visser M, et al

    . Establishing task- and modality-dependent dissociations between the semantic and default mode networks. Proc Natl Acad Sci U S A 2015;112:7857–62 doi:10.1073/pnas.1422760112 pmid:26056304

    Abstract/FREE Full Text
22. 22.↵
    2. Ojemann JG,
    3. Buckner RL,
    4. Akbudak E, et al

    . Functional MRI studies of word-stem completion: reliability across laboratories and comparison to blood flow imaging with PET. Hum Brain Mapp 1998;6:203–15 pmid:9704261

    CrossRefPubMedWeb of Science
23. 23.↵
    2. Casella JF,
    3. King AA,
    4. Barton B, et al

    . Design of the silent cerebral infarct transfusion (SIT) trial. Pediatr Hematol Oncol 2010;27:69–89 doi:10.3109/08880010903360367 pmid:20201689

    CrossRefPubMedWeb of Science
24. 24.↵
    2. Bush AM,
    3. Borzage MT,
    4. Choi S, et al

    . Determinants of resting cerebral blood flow in sickle cell disease. Am J Hematol 2016;91:912–17 doi:10.1002/ajh.24441 pmid:27263497

    CrossRefPubMed
25. 25.↵
    2. Raichle ME,
    3. Snyder AZ

    . A default mode of brain function: a brief history of an evolving idea. Neuroimage 2007;37:1083–90; discussion 1097–99 doi:10.1016/j.neuroimage.2007.02.041 pmid:17719799

    CrossRefPubMedWeb of Science
26. 26.↵
    2. Kim JA,
    3. Leung J,
    4. Lerch JP, et al

    . Reduced cerebrovascular reserve is regionally associated with cortical thickness reductions in children with sickle cell disease. Brain Res 2016;1642:263–69 doi:10.1016/j.brainres.2016.03.041 pmid:27026656

    CrossRefPubMed
27. 27.↵
    2. Jordan LC,
    3. Gindville MC,
    4. Scott AO, et al

    . Non-invasive imaging of oxygen extraction fraction in adults with sickle cell anaemia. Brain 2016;139:738–50 doi:10.1093/brain/awv397 pmid:26823369

    Abstract/FREE Full Text
28. 28.↵
    2. Kirk GR,
    3. Haynes MR,
    4. Palasis S, et al

    . Regionally specific cortical thinning in in children with sickle cell disease. Cereb Cortex 2009;19:1549–56 doi:10.1093/cercor/bhn193 pmid:18996911

    Abstract/FREE Full Text