BACKGROUND: Little is known about cerebral blood flow (CBF) in young patients with ischemic stroke caused by an intracranial arteriopathy. Arterial spin labeling (ASL) perfusion is a noninvasive technique for measuring CBF. We aimed to investigate whether, in young patients with unilateral intracranial arteriopathy and previous ischemic stroke, CBF is compromised in noninfarcted brain areas of the symptomatic hemisphere and whether this is related to the severity of the arteriopathy. METHODS: Patients aged 5-50 years, with previous middle cerebral artery (MCA) territory infarction and a unilateral intracranial arteriopathy, underwent magnetic resonance imaging (MRI), MR angiography and pseudocontinuous ASL perfusion MRI. We assessed the severity of stenosis of arteries that fed the symptomatic MCA territory, quantified CBF in the noninfarcted cortex of both MCA territories and generated CBF maps for visual CBF interpretation. RESULTS: A total of 17 patients were included (median age 29 years, range 5-49, 29% male). We found a similar median quantified CBF in the symptomatic and asymptomatic MCA territories (86 ml·100 g(-1)·min(-1)). CBF maps showed hypoperfusion in the symptomatic MCA territory in 59% of patients compared to 18% based on quantified CBF. Patients with a severe arteriopathy more often showed hypoperfusion on CBF maps than patients with a mild arteriopathy. In 53% of patients, small foci of increased signal intensity were visible on CBF maps around an area of hypoperfusion, indicating vascular artifacts. In these patients, we found large intraindividual variation in the quantified CBF in the symptomatic hemisphere. In 47% of patients, the visual interpretation of perfusion did not correspond with the quantified CBF. CONCLUSIONS: This study shows that more than half of young patients with previous ischemic stroke in the MCA territory and a unilateral intracranial arteriopathy have hypoperfusion in the noninfarcted cortex of the symptomatic hemisphere when CBF is visually assessed using a CBF map, in particular in patients with a severe arteriopathy. In the same patients, quantification of CBF shows hypoperfusion in the symptomatic hemisphere in only 18%. This discrepancy is caused by labeled blood within the arteries that has not yet reached the tissue at the time of imaging. Visual assessment can show hypoperfusion, while the quantified CBF in a similar region appears higher when the intravascular labeled blood is included in the region of interest. Further research should focus on elucidating whether cerebral perfusion deficits in young stroke patients with intracranial arteriopathy might help to identify patients who are at risk of poor outcome or stroke recurrence.
BACKGROUND: Little is known about cerebral blood flow (CBF) in young patients with ischemic stroke caused by an intracranial arteriopathy. Arterial spin labeling (ASL) perfusion is a noninvasive technique for measuring CBF. We aimed to investigate whether, in young patients with unilateral intracranial arteriopathy and previous ischemic stroke, CBF is compromised in noninfarcted brain areas of the symptomatic hemisphere and whether this is related to the severity of the arteriopathy. METHODS:Patients aged 5-50 years, with previous middle cerebral artery (MCA) territory infarction and a unilateral intracranial arteriopathy, underwent magnetic resonance imaging (MRI), MR angiography and pseudocontinuous ASL perfusion MRI. We assessed the severity of stenosis of arteries that fed the symptomatic MCA territory, quantified CBF in the noninfarcted cortex of both MCA territories and generated CBF maps for visual CBF interpretation. RESULTS: A total of 17 patients were included (median age 29 years, range 5-49, 29% male). We found a similar median quantified CBF in the symptomatic and asymptomatic MCA territories (86 ml·100 g(-1)·min(-1)). CBF maps showed hypoperfusion in the symptomatic MCA territory in 59% of patients compared to 18% based on quantified CBF. Patients with a severe arteriopathy more often showed hypoperfusion on CBF maps than patients with a mild arteriopathy. In 53% of patients, small foci of increased signal intensity were visible on CBF maps around an area of hypoperfusion, indicating vascular artifacts. In these patients, we found large intraindividual variation in the quantified CBF in the symptomatic hemisphere. In 47% of patients, the visual interpretation of perfusion did not correspond with the quantified CBF. CONCLUSIONS: This study shows that more than half of young patients with previous ischemic stroke in the MCA territory and a unilateral intracranial arteriopathy have hypoperfusion in the noninfarcted cortex of the symptomatic hemisphere when CBF is visually assessed using a CBF map, in particular in patients with a severe arteriopathy. In the same patients, quantification of CBF shows hypoperfusion in the symptomatic hemisphere in only 18%. This discrepancy is caused by labeled blood within the arteries that has not yet reached the tissue at the time of imaging. Visual assessment can show hypoperfusion, while the quantified CBF in a similar region appears higher when the intravascular labeled blood is included in the region of interest. Further research should focus on elucidating whether cerebral perfusion deficits in young strokepatients with intracranial arteriopathy might help to identify patients who are at risk of poor outcome or stroke recurrence.