期刊
BRAIN AND BEHAVIOR
卷 11, 期 3, 页码 -出版社
WILEY
DOI: 10.1002/brb3.1978
关键词
microstructural damage; neurocognitive; sickle cell disease; tract-specific analysis; white matter
资金
- National Heart Lung and Blood Institute [1U01HL117718-01, 1RO1HL136484-A1]
- National Center for Research Resources [UL1 TR001855-02]
- National Institute of Neurological Disorders and Stroke [1F31NS106828-01A1]
- National Institute of Biomedical Imaging and Bioengineering [3R01EB025032]
- Saban Research Institute [000013228]
Sickle cell disease (SCD) is a hereditary blood disorder characterized by abnormal hemoglobin molecules in red blood cells. Patients with SCD are at increased risk for strokes and neurocognitive deficits. The study utilized tract-specific analysis (TSA) to evaluate white matter (WM) damage in SCD patients and found disruptions in WM microstructure metrics, particularly in the corpus callosum and other major WM tracts.
Introduction: Sickle cell disease (SCD) is a hereditary blood disorder in which the oxygen-carrying hemoglobin molecule in red blood cells is abnormal. SCD patients are at increased risks for strokes and neurocognitive deficit, even though neurovascular screening and treatments have lowered the rate of overt strokes. Tract-specific analysis (TSA) is a statistical method to evaluate microstructural WM damage in neurodegenerative disorders, using diffusion tensor imaging (DTI). Methods: We utilized TSA and compared 11 major brain WM tracts between SCD patients with no history of overt stroke, anemic controls, and healthy controls. We additionally examined the relationship between the most commonly used DTI metric of WM tracts and neurocognitive performance in the SCD patients and healthy controls. Results: Disruption of WM microstructure orientation-dependent metrics for the SCD patients was found in the genu of the corpus callosum (CC), cortico-spinal tract, inferior fronto-occipital fasciculus, right inferior longitudinal fasciculus, superior longitudinal fasciculus, and left uncinate fasciculus. Neurocognitive performance indicated slower processing speed and lower response inhibition skills in SCD patients compared to controls. TSA abnormalities in the CC were significantly associated with measures of processing speed, working memory, and executive functions. Conclusion: Decreased DTI-derived metrics were observed on six tracts in chronically anemic patients, regardless of anemia subtype, while two tracks with decreased measures were unique to SCD patients. Patients with WMHs had more significant FA abnormalities. Decreased FA values in the CC significantly correlated with all nine neurocognitive tests, suggesting a critical importance for CC in core neurocognitive processes.
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