Impaired iron metabolism and cerebral perfusion patterns in unilateral middle cerebral artery stenosis or occlusion: Insights from quantitative susceptibility mapping.

Background and purpose: Cerebral hypoperfusion caused by stenosis or occlusion of the middle cerebral artery (MCA) may be followed by impaired iron metabolism. We explored the association between iron changes of gray matter (GM) nuclei subregions and different cerebral perfusion patterns in patients with chronic unilateral middle cerebral artery (MCA) stenosis or occlusion using quantitative susceptibility imaging (QSM).

Methods: Sixty-one patients with unilateral MCA stenosis or occlusion were recruited and scored with Alberta-Stroke-Program-Early-CT-Score (ASPECTS) based on relative cerebral blood flow (rCBF) measurements to calculate the number of corresponding hypoperfusion subregions, and then divided into an extensive-hypoperfusion group (EH group), regional-hypoperfusion group (RH group), and normal-perfusion group (Control group) accordingly. The measured magnetic susceptibility of GM nuclei subregions was compared between the lesion and contralateral side for each group and among the three groups. Correlation analysis was performed to assess the relationships of magnetic susceptibility of GM nuclei with mean rCBF, National-Institutes-of-Health-stroke-scale (NIHSS) and modified-Rankin-scale (mRS) scores.

Results: Magnetic susceptibility in the putamen (PU) and globus pallidus (GP) at the lesion side was higher in the EH and RH groups compared with the contralateral side (all P < 0.05). Susceptibility in the lesion side PU and GP showed negative correlations with mean rCBF and positive correlations with NIHSS and mRS scores (all P < 0.05).

Conclusion: Our findings demonstrate that chronic cerebral hypoperfusion might be one cause of cerebral abnormal iron metabolism. In addition, magnetic susceptibility of PU and GP seems to be correlated with stroke scale scores, suggesting that iron deposition may play an important role in neurologic deficits after ischemic stroke.