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An arterial spin labeling investigation of cerebral blood flow deficits in chronic stroke survivors
An arterial spin labeling investigation of cerebral blood flow deficits in chronic stroke survivors
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An arterial spin labeling investigation of cerebral blood flow deficits in chronic stroke survivors
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An arterial spin labeling investigation of cerebral blood flow deficits in chronic stroke survivors
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An arterial spin labeling investigation of cerebral blood flow deficits in chronic stroke survivors
An arterial spin labeling investigation of cerebral blood flow deficits in chronic stroke survivors
Journal Article

An arterial spin labeling investigation of cerebral blood flow deficits in chronic stroke survivors

2010
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Overview
Although the acute stroke literature indicates that cerebral blood flow (CBF) may commonly be disordered in stroke survivors, limited research has investigated whether CBF remains aberrant in the chronic phase of stroke. A directed study of CBF in stroke is needed because reduced CBF (hypoperfusion) may occur in neural regions that appear anatomically intact and may impact cognitive functioning in stroke survivors. Hypoperfusion in neurologically-involved individuals may also affect BOLD signal in FMRI studies, complicating its interpretation with this population. The current study measured CBF in three chronic stroke survivors with ischemic infarcts (greater than 1year post-stroke) to localize regions of hypoperfusion, and most critically, examine the CBF inflow curve using a methodology that has never, to our knowledge, been reported in the chronic stroke literature. CBF data acquired with a Pulsed Arterial Spin Labeling (PASL) flow-sensitive alternating inversion recovery (FAIR) technique indicated both delayed CBF inflow curve and hypoperfusion in the stroke survivors as compared to younger and elderly control participants. Among the stroke survivors, we observed regional hypoperfusion in apparently anatomically intact neural regions that are involved in cognitive functioning. These results may have profound implications for the study of behavioral deficits in chronic stroke, and particularly for studies using neuroimaging methods that rely on CBF to draw conclusions about underlying neural activity.